Agents that increase calcium influx into calcium channels of excitable tissues. This causes vasoconstriction in VASCULAR SMOOTH MUSCLE and/or CARDIAC MUSCLE cells as well as stimulation of insulin release from pancreatic islets. Therefore, tissue-selective calcium agonists have the potential to combat cardiac failure and endocrinological disorders. They have been used primarily in experimental studies in cell and tissue culture.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue.
A calcium channel blocker with marked vasodilator action. It is an effective antihypertensive agent and differs from other calcium channel blockers in that it does not reduce glomerular filtration rate and is mildly natriuretic, rather than sodium retentive.
A potent antagonist of CALCIUM CHANNELS that is highly selective for VASCULAR SMOOTH MUSCLE. It is effective in the treatment of chronic stable angina pectoris, hypertension, and congestive cardiac failure.
Pyridine moieties which are partially saturated by the addition of two hydrogen atoms in any position.
Long-lasting voltage-gated CALCIUM CHANNELS found in both excitable and nonexcitable tissue. They are responsible for normal myocardial and vascular smooth muscle contractility. Five subunits (alpha-1, alpha-2, beta, gamma, and delta) make up the L-type channel. The alpha-1 subunit is the binding site for calcium-based antagonists. Dihydropyridine-based calcium antagonists are used as markers for these binding sites.
A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Gated, ion-selective glycoproteins that traverse membranes. The stimulus for ION CHANNEL GATING can be due to a variety of stimuli such as LIGANDS, a TRANSMEMBRANE POTENTIAL DIFFERENCE, mechanical deformation or through INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS.
A class of drugs that stimulate sodium influx through cell membrane channels.
CALCIUM CHANNELS that are concentrated in neural tissue. Omega toxins inhibit the actions of these channels by altering their voltage dependence.
A heterogenous group of transient or low voltage activated type CALCIUM CHANNELS. They are found in cardiac myocyte membranes, the sinoatrial node, Purkinje cells of the heart and the central nervous system.
Signal transduction mechanisms whereby calcium mobilization (from outside the cell or from intracellular storage pools) to the cytoplasm is triggered by external stimuli. Calcium signals are often seen to propagate as waves, oscillations, spikes, sparks, or puffs. The calcium acts as an intracellular messenger by activating calcium-responsive proteins.
The opening and closing of ion channels due to a stimulus. The stimulus can be a change in membrane potential (voltage-gated), drugs or chemical transmitters (ligand-gated), or a mechanical deformation. Gating is thought to involve conformational changes of the ion channel which alters selective permeability.
Compounds that either stimulate the opening or prevent closure of VOLTAGE-GATED SODIUM CHANNELS.
A class of drugs that act by inhibition of potassium efflux through cell membranes. Blockade of potassium channels prolongs the duration of ACTION POTENTIALS. They are used as ANTI-ARRHYTHMIA AGENTS and VASODILATOR AGENTS.
Heteromultimers of Kir6 channels (the pore portion) and sulfonylurea receptor (the regulatory portion) which affect function of the HEART; PANCREATIC BETA CELLS; and KIDNEY COLLECTING DUCTS. KATP channel blockers include GLIBENCLAMIDE and mitiglinide whereas openers include CROMAKALIM and minoxidil sulfate.
A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of CALCIUM ion on membrane functions.
Potassium channels where the flow of K+ ions into the cell is greater than the outward flow.
CALCIUM CHANNELS located within the PURKINJE CELLS of the cerebellum. They are involved in stimulation-secretion coupling of neurons.
CALCIUM CHANNELS located in the neurons of the brain.
The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.
A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure.
A calcium channel blocker that is a class IV anti-arrhythmia agent.
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
CALCIUM CHANNELS located in the neurons of the brain. They are inhibited by the marine snail toxin, omega conotoxin MVIIC.
An electrophysiologic technique for studying cells, cell membranes, and occasionally isolated organelles. All patch-clamp methods rely on a very high-resistance seal between a micropipette and a membrane; the seal is usually attained by gentle suction. The four most common variants include on-cell patch, inside-out patch, outside-out patch, and whole-cell clamp. Patch-clamp methods are commonly used to voltage clamp, that is control the voltage across the membrane and measure current flow, but current-clamp methods, in which the current is controlled and the voltage is measured, are also used.
Cell membrane glycoproteins that form channels to selectively pass chloride ions. Nonselective blockers include FENAMATES; ETHACRYNIC ACID; and TAMOXIFEN.
A guanidine that opens POTASSIUM CHANNELS producing direct peripheral vasodilatation of the ARTERIOLES. It reduces BLOOD PRESSURE and peripheral resistance and produces fluid retention. (Martindale The Extra Pharmacopoeia, 31st ed)
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
An element of the alkaline earth group of metals. It has an atomic symbol Ba, atomic number 56, and atomic weight 138. All of its acid-soluble salts are poisonous.
A neurotoxic peptide, which is a cleavage product (VIa) of the omega-Conotoxin precursor protein contained in venom from the marine snail, CONUS geographus. It is an antagonist of CALCIUM CHANNELS, N-TYPE.
The relationship between the dose of an administered drug and the response of the organism to the drug.
The ability of a substrate to allow the passage of ELECTRONS.
Calcium compounds used as food supplements or in food to supply the body with calcium. Dietary calcium is needed during growth for bone development and for maintenance of skeletal integrity later in life to prevent osteoporosis.
The rate dynamics in chemical or physical systems.
Compounds that either stimulate the opening or prevent closure of EPITHELIAL SODIUM ION CHANNELS.
A family of structurally related neurotoxic peptides from mollusk venom that inhibit voltage-activated entry of calcium into the presynaptic membrane. They selectively inhibit N-, P-, and Q-type calcium channels.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
Potassium channel whose permeability to ions is extremely sensitive to the transmembrane potential difference. The opening of these channels is induced by the membrane depolarization of the ACTION POTENTIAL.
An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
Potassium channels whose activation is dependent on intracellular calcium concentrations.
An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
A derivative of the NIACINAMIDE that is structurally combined with an organic nitrate. It is a potassium-channel opener that causes vasodilatation of arterioles and large coronary arteries. Its nitrate-like properties produce venous vasodilation through stimulation of guanylate cyclase.
A potassium-channel opening vasodilator that has been investigated in the management of hypertension. It has also been tried in patients with asthma. (Martindale, The Extra Pharmacopoeia, 30th ed, p352)
A benzimidazoyl-substituted tetraline that selectively binds and inhibits CALCIUM CHANNELS, T-TYPE.
A class of drugs that act by inhibition of sodium influx through cell membranes. Blockade of sodium channels slows the rate and amplitude of initial rapid depolarization, reduces cell excitability, and reduces conduction velocity.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
An autoimmune disease characterized by weakness and fatigability of proximal muscles, particularly of the pelvic girdle, lower extremities, trunk, and shoulder girdle. There is relative sparing of extraocular and bulbar muscles. CARCINOMA, SMALL CELL of the lung is a frequently associated condition, although other malignancies and autoimmune diseases may be associated. Muscular weakness results from impaired impulse transmission at the NEUROMUSCULAR JUNCTION. Presynaptic calcium channel dysfunction leads to a reduced amount of acetylcholine being released in response to stimulation of the nerve. (From Adams et al., Principles of Neurology, 6th ed, pp 1471)
Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.
A subgroup of TRP cation channels that contain 3-4 ANKYRIN REPEAT DOMAINS and a conserved C-terminal domain. Members are highly expressed in the CENTRAL NERVOUS SYSTEM. Selectivity for calcium over sodium ranges from 0.5 to 10.
A neuropeptide toxin from the venom of the funnel web spider, Agelenopsis aperta. It inhibits CALCIUM CHANNELS, P-TYPE by altering the voltage-dependent gating so that very large depolarizations are needed for channel opening. It also inhibits CALCIUM CHANNELS, Q-TYPE.
A benzoate-cevane found in VERATRUM and Schoenocaulon. It activates SODIUM CHANNELS to stay open longer than normal.
Voltage-gated potassium channels whose primary subunits contain six transmembrane segments and form tetramers to create a pore with a voltage sensor. They are related to their founding member, shaker protein, Drosophila.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
Elements of limited time intervals, contributing to particular results or situations.
Drugs that bind to and activate dopamine receptors.
A white crystal or crystalline powder used in BUFFERS; FERTILIZERS; and EXPLOSIVES. It can be used to replenish ELECTROLYTES and restore WATER-ELECTROLYTE BALANCE in treating HYPOKALEMIA.
The hollow, muscular organ that maintains the circulation of the blood.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
A major class of calcium activated potassium channels whose members are voltage-dependent. MaxiK channels are activated by either membrane depolarization or an increase in intracellular Ca(2+). They are key regulators of calcium and electrical signaling in a variety of tissues.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Compounds with a core of fused benzo-pyran rings.
Use of electric potential or currents to elicit biological responses.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Female germ cells derived from OOGONIA and termed OOCYTES when they enter MEIOSIS. The primary oocytes begin meiosis but are arrested at the diplotene state until OVULATION at PUBERTY to give rise to haploid secondary oocytes or ova (OVUM).
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
A subgroup of TRP cation channels named after vanilloid receptor. They are very sensitive to TEMPERATURE and hot spicy food and CAPSAICIN. They have the TRP domain and ANKYRIN repeats. Selectivity for CALCIUM over SODIUM ranges from 3 to 100 fold.
Established cell cultures that have the potential to propagate indefinitely.
Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement.
The commonest and widest ranging species of the clawed "frog" (Xenopus) in Africa. This species is used extensively in research. There is now a significant population in California derived from escaped laboratory animals.
A subgroup of cyclic nucleotide-regulated ION CHANNELS within the superfamily of pore-loop cation channels. They are expressed in OLFACTORY NERVE cilia and in PHOTORECEPTOR CELLS and some PLANTS.
A salt used to replenish calcium levels, as an acid-producing diuretic, and as an antidote for magnesium poisoning.
Cell membrane glycoproteins that are selectively permeable to potassium ions. At least eight major groups of K channels exist and they are made up of dozens of different subunits.
Contractile activity of the MYOCARDIUM.
A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.
The nonstriated involuntary muscle tissue of blood vessels.
A tetrameric calcium release channel in the SARCOPLASMIC RETICULUM membrane of SMOOTH MUSCLE CELLS, acting oppositely to SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES. It is important in skeletal and cardiac excitation-contraction coupling and studied by using RYANODINE. Abnormalities are implicated in CARDIAC ARRHYTHMIAS and MUSCULAR DISEASES.
A methylpyrrole-carboxylate from RYANIA that disrupts the RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL to modify CALCIUM release from SARCOPLASMIC RETICULUM resulting in alteration of MUSCLE CONTRACTION. It was previously used in INSECTICIDES. It is used experimentally in conjunction with THAPSIGARGIN and other inhibitors of CALCIUM ATPASE uptake of calcium into SARCOPLASMIC RETICULUM.
A subgroup of TRP cation channels named after melastatin protein. They have the TRP domain but lack ANKYRIN repeats. Enzyme domains in the C-terminus leads to them being called chanzymes.
Venoms of arthropods of the order Araneida of the ARACHNIDA. The venoms usually contain several protein fractions, including ENZYMES, hemolytic, neurolytic, and other TOXINS, BIOLOGICAL.
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
A family of proton-gated sodium channels that are primarily expressed in neuronal tissue. They are AMILORIDE-sensitive and are implicated in the signaling of a variety of neurological stimuli, most notably that of pain in response to acidic conditions.

Melatonin inhibits release of luteinizing hormone (LH) via decrease of [Ca2+]i and cyclic AMP. (1/640)

The role of [Ca2+]i and cAMP in transduction of the melatonin inhibitory effect on GnRH-induced LH release from neonatal rat gonadotrophs has been studied, because melatonin inhibits the increase of both intracellular messengers. Treatments increasing Ca2+ influx (S(-) Bay K8644 or KCI) or cAMP concentration (8-bromo-cAMP or 3-isobutyl-1-methylxanthine) potentiated the GnRH-induced LH release and partially diminished the inhibitory effect of melatonin. Combination of the treatments increasing cAMP and calcium concentrations blocked completely the melatonin inhibition of LH release. The combined treatment with 8-bromo-cAMP and S(-) Bay K8644 also blocked the melatonin inhibition of GnRH-induced [Ca2+]i increase in 89 % of the gonadotrophs, while any of the treatments alone blocked the melatonin effect in about 25 % of these cells. These observations suggest that a cAMP-dependent pathway is involved in regulation of Ca2+ influx by melatonin and melatonin inhibition of LH release may be mediated by the decrease of both messengers.  (+info)

Intracellular Ca2+ concentrations in cultured chicken photoreceptor cells: sustained elevation in depolarized cells and the role of dihydropyridine-sensitive Ca2+ channels. (2/640)

PURPOSE: Retinal photoreceptor cells are tonically depolarized in darkness. Ca2+ influx in darkness plays a critical role in the regulation of neurotransmitter release and melatonin synthesis in these sensory cells. The purpose of the present study was to examine the dynamic changes of intracellular Ca2+ concentrations ([Ca2+]in ) in response to a tonic depolarizing stimulus and to determine the role of dihydropyridine-sensitive calcium channels in the response. METHODS: Photoreceptor cells were prepared from embryonic chick retina and cultured for 6-12 days. Cells were depolarized by exposure to 35 mM extracellular K+. [Ca2+]in of individual photoreceptor cell bodies/synaptic terminals was determined by ratiometric fura-2 image analysis. RESULTS: Chemical depolarization with 35 mM [K+]out greatly increased [Ca2+]in of inner segment/synaptic terminal regions of photoreceptors. The increase usually reached a plateau after the first few minutes of stimulation and was sustained for prolonged periods (>2 h) in the presence of high K+. When the extracellular K+ concentration was reduced, the [Ca2+]in rapidly returned to the basal level. Substitution of 1 mM CoCl2 for CaCl2 in the superfusion medium rapidly and reversibly reduced the [Ca2+]in of depolarized photoreceptor cells. Antagonists of L-type Ca2+ channels, nitrendipine and nifedipine, inhibited the K+-evoked increase of [Ca2+]in. Bay K 8644, a dihydropyridine Ca2+ channel agonist, potentiated the increase of [Ca2+]in elicited by high K+. In some cells, Bay K 8644 alone increased [Ca2+]in under basal conditions. CONCLUSIONS: The increase of [Ca2+]in elicited by depolarization with 35 mM extracellular K+ is due to influx of calcium through the dihydropyridine-sensitive voltage-gated channels. Intracellular [Ca2+] remains elevated for extended periods of time during tonic depolarization. This sustained response requires continuous Ca2+ channel activity.  (+info)

Voltage inactivation of Ca2+ entry and secretion associated with N- and P/Q-type but not L-type Ca2+ channels of bovine chromaffin cells. (3/640)

1. In this study we pose the question of why the bovine adrenal medullary chromaffin cell needs various subtypes (L, N, P, Q) of the neuronal high-voltage activated Ca2+ channels to control a given physiological function, i.e. the exocytotic release of catecholamines. One plausible hypothesis is that Ca2+ channel subtypes undergo different patterns of inactivation during cell depolarization. 2. The net Ca2+ uptake (measured using 45Ca2+) into hyperpolarized cells (bathed in a nominally Ca2+-free solution containing 1.2 mM K+) after application of a Ca2+ pulse (5 s exposure to 100 mM K+ and 2 mM Ca2+), amounted to 0.65 +/- 0.02 fmol cell-1; in depolarized cells (bathed in nominally Ca2+-free solution containing 100 mM K+) the net Ca2+ uptake was 0.16 +/- 0.01 fmol cell-1. 3. This was paralleled by a dramatic reduction of the increase in the cytosolic Ca2+ concentration, [Ca2+]i, caused by Ca2+ pulses applied to fura-2-loaded single cells, from 1181 +/- 104 nM in hyperpolarized cells to 115 +/- 9 nM in depolarized cells. 4. A similar decrease was observed when studying catecholamine release. Secretion was decreased when K+ concentration was increased from 1.2 to 100 mM; the Ca2+ pulse caused, when comparing the extreme conditions, the secretion of 807 +/- 35 nA of catecholamines in hyperpolarized cells and 220 +/- 19 nA in depolarized cells. 5. The inactivation by depolarization of Ca2+ entry and secretion occluded the blocking effects of combined omega-conotoxin GVIA (1 microM) and omega-agatoxin IVA (2 microM), thus suggesting that depolarization caused a selective inactivation of the N- and P/Q-type Ca2+ channels. 6. This was strengthened by two additional findings: (i) nifedipine (3 microM), an L-type Ca2+ channel blocker, suppressed the fraction of Ca2+ entry (24 %) and secretion (27 %) left unblocked by depolarization; (ii) FPL64176 (3 microM), an L-type Ca2+ channel 'activator', dramatically enhanced the entry of Ca2+ and the secretory response in depolarized cells. 7. In voltage-clamped cells, switching the holding potential from -80 to -40 mV promoted the loss of 80 % of the whole-cell inward Ca2+ channel current carried by 10 mM Ba2+ (IBa). The residual current was blocked by 80 % upon addition of 3 microM nifedipine and dramatically enhanced by 3 microM FPL64176. 8. Thus, it seems that the N- and P/Q-subtypes of calcium channels are more prone to inactivation at depolarizing voltages than the L-subtype. We propose that this different inactivation might occur physiologically during different patterns of action potential firing, triggered by endogenously released acetylcholine under various stressful conditions.  (+info)

A new scorpion toxin (BmK-PL) stimulates Ca2+-release channel activity of the skeletal-muscle ryanodine receptor by an indirect mechanism. (4/640)

A peptide toxin isolated from the Chinese scorpion Buthus martensi Karsch (BmK-PL) stimulated Ca2+-release channel activity in both triad membranes and reconstituted ryanodine receptors partially purified from rabbit skeletal muscle. In [3H]ryanodine binding experiments, the toxin increased the affinity of ryanodine for the receptor, from a Kd of 24.3 nM to 2.9 nM, which is an enhancement similar to that seen with known receptor activators, such as ATP and high concentrations of KCl. In contrast, toxin enhancement was not observed with purified receptors, although intrinsic binding activity and stimulation by the conventional receptor activators were retained. In single channel recordings of Ca2+-release activity, the toxin increased the open channel probability (Po) from 0.019 to 0.043 (226% of control) in triad preparations. Further toxin enhancement of Po from 0.07 to 0.37 (529% of control) was observed using partially-purified receptors in the presence of ATP. When purified receptors were assayed in the presence of ATP, however, they showed a high value of Po (0.33) and no further increase was observed following application of the toxin. Results derived from two different experimental methods consistently suggest that a molecule(s) required for toxin-induced enhancement is absent from the purified receptor preparation. Western blot analysis of receptors prepared using three different protocols showed that triadin was missing from the purified receptor preparation. The scorpion toxin minimally enhanced Ca2+-release channel activity of cardiac preparations. From these results, we conclude that the toxin preferentially increases the activity of skeletal-muscle ryanodine receptors by an indirect mechanism, possibly binding to associated protein molecule(s). Triadin is a strong candidate for such a molecule.  (+info)

BAY K 8644 modifies Ca2+ cross signaling between DHP and ryanodine receptors in rat ventricular myocytes. (5/640)

The amplification factor of dihydropyridine (DHP)/ryanodine receptors was defined as the amount of Ca2+ released from the sarcoplasmic reticulum (SR) relative to the influx of Ca2+ through L-type Ca2+ channels in rat ventricular myocytes. The amplification factor showed steep voltage dependence at potentials negative to -10 mV but was less dependent on voltage at potentials positive to this value. In cells dialyzed with 0.2 mM cAMP in addition to 2 mM fura 2, the Ca2+-channel agonist (-)-BAY K 8644 enhanced Ca2+-channel current (ICa), shifted the activation curve by -10 mV, and significantly delayed its inactivation. Surprisingly, BAY K 8644 reduced the amplification factor by 50% at all potentials, even though the caffeine-releasable Ca2+ stores were mostly intact at holding potentials of -90 mV. In contrast, brief elevation of extracellular Ca2+ activity from 2 to 10 mM enhanced both ICa and intracellular Ca2+ transients in the absence or presence of BAY K 8644 but had no significant effect on the amplification factor. BAY K 8644 abolished the direct dependence of the rate of inactivation of ICa on the release of Ca2+ from the SR. These findings suggest that the gain of the Ca2+-induced Ca2+ release in cardiac myocytes is regulated by the gating kinetics of cardiac L-type Ca2+ channels via local exchange of Ca2+ signals between DHP and ryanodine receptors and that BAY K 8644 suppresses the amplification factor through attenuation of the Ca2+-dependent inactivation of Ca2+ channels.  (+info)

Inositol 1,3,4,5-tetrakisphosphate enhances long-term potentiation by regulating Ca2+ entry in rat hippocampus. (6/640)

1. The effect of inositol 1,3,4,5-tetrakisphosphate (InsP4) on long-term potentiation (LTP) was investigated in the CA1 region of rat hippocampal slices. Intracellular application of InsP4 and EPSP recordings were carried out using the whole-cell configuration. 2. Induction of LTP in the presence of InsP4 (100 microM) resulted in a substantial enhancement of the LTP magnitude compared with control potentiation. Using an intrapipette perfusion system, it was established that application of InsP4 was required during induction of potentiation for this enhancement to occur. An enhancement of LTP was not observed if a non-metabolizable inositol 1,4,5-trisphosphate (InsP3) analogue (2,3-dideoxy-1,4,5-trisphosphate, 100 microM) was applied intracellularly. 3. Current-voltage relations of NMDA receptor-mediated EPSCs were not altered by InsP4 application. The presence of InsP4 was slightly effective in relieving a D-(-)-2-amino-5-phosphonopentanoic acid (D-APV)-induced block of LTP. 4. The peak current amplitude of voltage-gated calcium channels (VGCCs) was increased by InsP4. omega-Conotoxin GVIA inhibited the InsP4-induced LTP facilitation. 5. These data indicate that InsP4 can modify the extracellular Ca2+ entry through upregulation of VGCCs, which may in turn contribute to the observed enhancement of LTP induced by InsP4. 6. To investigate the possible involvement of intracellular Ca2+ release in the facilitatory effect of InsP4 on LTP, different inhibitors of the endoplasmic reticulum-dependent Ca2+ release were applied (heparin, ryanodine, cyclopiazonic acid). The results suggest that InsP4 activates postsynaptic InsP3-dependent Ca2+ release which normally does not contribute to the calcium-induced calcium release-dependent LTP.  (+info)

Differentially expressed genes in C6.9 glioma cells during vitamin D-induced cell death program. (7/640)

C6.9 rat glioma cells undergo a cell death program when exposed to 1, 25-dihydroxyvitamin D3 (1,25-D3). As a global analytical approach, we have investigated gene expression in C6.9 engaged in this cell death program using differential screening of a rat brain cDNA library with probes derived from control and 1,25-D3-treated cells. Using this methodology we report the isolation of 61 differentially expressed cDNAs. Forty-seven cDNAs correspond to genes already characterized in rat cells or tissues. Seven cDNAs are homologous to yeast, mouse or human genes and seven are not related to known genes. Some of the characterized genes have been reported to be differentially expressed following induction of programmed cell death. These include PMP22/gas3, MGP and beta-tubulin. For the first time, we also show a cell death program induced up-regulation of the c-myc associated primary response gene CRP, and of the proteasome RN3 subunit and TCTP/mortalin genes. Another interesting feature of this 1,25-D3 induced-cell death program is the down-regulated expression of transcripts for the microtubule motor dynein heavy chain/MAP 1C and of the calcium-binding S100beta protein. Finally 15 upregulated cDNAs encode ribosomal proteins suggesting a possible involvement of the translational apparatus in this cell program. Alternatively, these ribosomal protein genes could be up-regulated in response to altered rates of cellular metabolism, as has been demonstrated for most of the other isolated genes which encode proteins involved in metabolic pathways. Thus, this study presents to our knowledge the first characterization of genes which are differentially expressed during a cell death program induced by 1, 25-D3. Therefore, this data provides new information on the fundamental mechanisms which participate in the antineoplastic effects of 1,25-D3 and on the machinery of a cell death program in a glioma cell line.  (+info)

Bicarbonate and chloride secretion in Calu-3 human airway epithelial cells. (8/640)

Serous cells are the predominant site of cystic fibrosis transmembrane conductance regulator expression in the airways, and they make a significant contribution to the volume, composition, and consistency of the submucosal gland secretions. We have employed the human airway serous cell line Calu-3 as a model system to investigate the mechanisms of serous cell anion secretion. Forskolin-stimulated Calu-3 cells secrete HCO-3 by a Cl-offdependent, serosal Na+-dependent, serosal bumetanide-insensitive, and serosal 4,4'-dinitrostilben-2,2'-disulfonic acid (DNDS)-sensitive, electrogenic mechanism as judged by transepithelial currents, isotopic fluxes, and the results of ion substitution, pharmacology, and pH studies. Similar studies revealed that stimulation of Calu-3 cells with 1-ethyl-2-benzimidazolinone (1-EBIO), an activator of basolateral membrane Ca2+-activated K+ channels, reduced HCO-3 secretion and caused the secretion of Cl- by a bumetanide-sensitive, electrogenic mechanism. Nystatin permeabilization of Calu-3 monolayers demonstrated 1-EBIO activated a charybdotoxin- and clotrimazole- inhibited basolateral membrane K+ current. Patch-clamp studies confirmed the presence of an intermediate conductance inwardly rectified K+ channel with this pharmacological profile. We propose that hyperpolarization of the basolateral membrane voltage elicits a switch from HCO-3 secretion to Cl- secretion because the uptake of HCO-3 across the basolateral membrane is mediated by a 4,4 '-dinitrostilben-2,2'-disulfonic acid (DNDS)-sensitive Na+:HCO-3 cotransporter. Since the stoichiometry reported for Na+:HCO-3 cotransport is 1:2 or 1:3, hyperpolarization of the basolateral membrane potential by 1-EBIO would inhibit HCO-3 entry and favor the secretion of Cl-. Therefore, differential regulation of the basolateral membrane K+ conductance by secretory agonists could provide a means of stimulating HCO-3 and Cl- secretion. In this context, cystic fibrosis transmembrane conductance regulator could serve as both a HCO-3 and a Cl- channel, mediating the apical membrane exit of either anion depending on basolateral membrane anion entry mechanisms and the driving forces that prevail. If these results with Calu-3 cells accurately reflect the transport properties of native submucosal gland serous cells, then HCO-3 secretion in the human airways warrants greater attention.  (+info)

Calcium channel agonists are substances that increase the activity or function of calcium channels. Calcium channels are specialized proteins in cell membranes that regulate the flow of calcium ions into and out of cells. They play a crucial role in various physiological processes, including muscle contraction, hormone secretion, and nerve impulse transmission.

Calcium channel agonists can enhance the opening of these channels, leading to an increased influx of calcium ions into the cells. This can result in various pharmacological effects, depending on the type of cell and tissue involved. For example, calcium channel agonists may be used to treat conditions such as hypotension (low blood pressure) or heart block by increasing cardiac contractility and heart rate. However, these agents should be used with caution due to their potential to cause adverse effects, including increased heart rate, hypertension, and arrhythmias.

Examples of calcium channel agonists include drugs such as Bay K 8644, FPL 64176, and A23187. It's important to note that some substances can act as both calcium channel agonists and antagonists, depending on the dose, concentration, or duration of exposure.

Calcium channel blockers (CCBs) are a class of medications that work by inhibiting the influx of calcium ions into cardiac and smooth muscle cells. This action leads to relaxation of the muscles, particularly in the blood vessels, resulting in decreased peripheral resistance and reduced blood pressure. Calcium channel blockers also have anti-arrhythmic effects and are used in the management of various cardiovascular conditions such as hypertension, angina, and certain types of arrhythmias.

Calcium channel blockers can be further classified into two main categories based on their chemical structure: dihydropyridines (e.g., nifedipine, amlodipine) and non-dihydropyridines (e.g., verapamil, diltiazem). Dihydropyridines are more selective for vascular smooth muscle and have a greater effect on blood pressure than heart rate or conduction. Non-dihydropyridines have a more significant impact on cardiac conduction and contractility, in addition to their vasodilatory effects.

It is important to note that calcium channel blockers may interact with other medications and should be used under the guidance of a healthcare professional. Potential side effects include dizziness, headache, constipation, and peripheral edema.

Calcium channels are specialized proteins that span the membrane of cells and allow calcium ions (Ca²+) to flow in and out of the cell. They are crucial for many physiological processes, including muscle contraction, neurotransmitter release, hormone secretion, and gene expression.

There are several types of calcium channels, classified based on their biophysical and pharmacological properties. The most well-known are:

1. Voltage-gated calcium channels (VGCCs): These channels are activated by changes in the membrane potential. They are further divided into several subtypes, including L-type, P/Q-type, N-type, R-type, and T-type. VGCCs play a critical role in excitation-contraction coupling in muscle cells and neurotransmitter release in neurons.
2. Receptor-operated calcium channels (ROCCs): These channels are activated by the binding of an extracellular ligand, such as a hormone or neurotransmitter, to a specific receptor on the cell surface. ROCCs are involved in various physiological processes, including smooth muscle contraction and platelet activation.
3. Store-operated calcium channels (SOCCs): These channels are activated by the depletion of intracellular calcium stores, such as those found in the endoplasmic reticulum. SOCCs play a critical role in maintaining calcium homeostasis and signaling within cells.

Dysregulation of calcium channel function has been implicated in various diseases, including hypertension, arrhythmias, migraine, epilepsy, and neurodegenerative disorders. Therefore, calcium channels are an important target for drug development and therapy.

Nitrendipine is an antihypertensive drug, which belongs to the class of calcium channel blockers. It works by relaxing and widening the blood vessels, making it easier for the heart to pump blood and reducing the workload on the cardiovascular system. This helps to lower high blood pressure (hypertension) and improve overall cardiovascular health. Nitrendipine is available in oral tablet form and is typically prescribed by a healthcare professional for the treatment of hypertension.

It's important to note that this definition is intended to be a general overview of the medical use and properties of Nitrendipine, and it should not be used as a substitute for professional medical advice or treatment. Always consult with a qualified healthcare provider for information regarding any specific medical condition or treatment.

Isradipine is a medication that belongs to a class of drugs called calcium channel blockers. It works by relaxing the muscles of the blood vessels, which helps to lower blood pressure and improve the supply of oxygen and nutrients to the heart. Isradipine is used to treat high blood pressure (hypertension) and angina (chest pain).

The medical definition of Isradipine is:

A dihydropyridine calcium channel blocker, which is a selective inhibitor of calcium ion influx through the slow channels of cardiac and vascular muscle and is used in the treatment of hypertension and angina pectoris. The drug has positive inotropic effects on the heart and increases coronary blood flow. It has a rapid onset of action and a short elimination half-life, making it useful for the control of acute hypertensive episodes.

Dihydropyridines are a class of compounds that contain a core structure of two fused rings, each containing six carbon atoms, with a hydrogen atom attached to each of the two central carbon atoms. They are commonly used in pharmaceuticals, particularly as calcium channel blockers in the treatment of cardiovascular diseases.

Calcium channel blockers, including dihydropyridines, work by blocking the influx of calcium ions into cardiac and vascular smooth muscle cells. This leads to relaxation of the muscles, resulting in decreased peripheral resistance and reduced blood pressure. Dihydropyridines are known for their potent vasodilatory effects and include medications such as nifedipine, amlodipine, and felodipine.

It is important to note that while dihydropyridines can be effective in treating hypertension and angina, they may also have side effects such as headache, dizziness, and peripheral edema. Additionally, they may interact with other medications, so it is essential to consult a healthcare provider before starting or changing any medication regimen.

Calcium channels, L-type, are a type of voltage-gated calcium channel that are widely expressed in many excitable cells, including cardiac and skeletal muscle cells, as well as certain neurons. These channels play a crucial role in the regulation of various cellular functions, such as excitation-contraction coupling, hormone secretion, and gene expression.

L-type calcium channels are composed of five subunits: alpha-1, alpha-2, beta, gamma, and delta. The alpha-1 subunit is the pore-forming subunit that contains the voltage sensor and the selectivity filter for calcium ions. It has four repeated domains (I-IV), each containing six transmembrane segments (S1-S6). The S4 segment in each domain functions as a voltage sensor, moving outward upon membrane depolarization to open the channel and allow calcium ions to flow into the cell.

L-type calcium channels are activated by membrane depolarization and have a relatively slow activation and inactivation time course. They are also modulated by various intracellular signaling molecules, such as protein kinases and G proteins. L-type calcium channel blockers, such as nifedipine and verapamil, are commonly used in the treatment of hypertension, angina, and certain cardiac arrhythmias.

Nifedipine is an antihypertensive and calcium channel blocker medication. It works by relaxing the muscles of the blood vessels, which helps to lower blood pressure and improve the supply of oxygen and nutrients to the heart. Nifedipine is used to treat high blood pressure (hypertension), angina (chest pain), and certain types of heart rhythm disorders.

In medical terms, nifedipine can be defined as: "A dihydropyridine calcium channel blocker that is used in the treatment of hypertension, angina pectoris, and Raynaud's phenomenon. It works by inhibiting the influx of calcium ions into vascular smooth muscle and cardiac muscle, which results in relaxation of the vascular smooth muscle and decreased workload on the heart."

Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:

Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.

Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.

Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.

Ion channels are specialized transmembrane proteins that form hydrophilic pores or gaps in the lipid bilayer of cell membranes. They regulate the movement of ions (such as sodium, potassium, calcium, and chloride) across the cell membrane by allowing these charged particles to pass through selectively in response to various stimuli, including voltage changes, ligand binding, mechanical stress, or temperature changes. This ion movement is essential for many physiological processes, including electrical signaling, neurotransmission, muscle contraction, and maintenance of resting membrane potential. Ion channels can be categorized based on their activation mechanisms, ion selectivity, and structural features. Dysfunction of ion channels can lead to various diseases, making them important targets for drug development.

Sodium channel agonists are substances that enhance the activity or function of sodium channels. Sodium channels are membrane proteins that play a crucial role in the generation and transmission of electrical signals in excitable cells, such as nerve and muscle cells. They allow the influx of sodium ions into the cell, which leads to the depolarization of the cell membrane and the initiation of an action potential.

Sodium channel agonists increase the likelihood, duration, or amplitude of action potentials by promoting the opening of sodium channels or slowing their closure. These effects can have various physiological consequences depending on the type of cell and tissue involved. In some cases, sodium channel agonists may be used for therapeutic purposes, such as in the treatment of certain types of heart arrhythmias. However, they can also have harmful or toxic effects, especially when used in excessive amounts or in sensitive populations.

Examples of sodium channel agonists include some drugs used to treat cardiac arrhythmias, such as Class I antiarrhythmic agents like ajmaline, flecainide, and procainamide. These drugs bind to the sodium channels and stabilize their open state, reducing the frequency and velocity of action potentials in the heart. Other substances that can act as sodium channel agonists include certain neurotoxins, such as batrachotoxin and veratridine, which are found in some species of plants and animals and can have potent effects on nerve and muscle function.

Calcium channels, N-type ( Cav2.2) are voltage-gated calcium channels found in excitable cells such as neurons and cardiac myocytes. They play a crucial role in regulating various cellular functions, including neurotransmitter release, gene expression, and cell excitability.

N-type calcium channels are composed of five subunits: an alpha1 (Cav2.2) subunit that forms the ion-conducting pore, and four auxiliary subunits (alpha2delta, beta, and gamma) that modulate channel function and stability. The alpha1 subunit contains the voltage sensor and the selectivity filter for calcium ions.

N-type calcium channels are activated by depolarization of the cell membrane and mediate a rapid influx of calcium ions into the cytoplasm. This calcium influx triggers neurotransmitter release from presynaptic terminals, regulates gene expression in the nucleus, and contributes to the electrical excitability of neurons.

N-type calcium channels are also targets for various drugs and toxins that modulate their activity. For example, the peptide toxin from cone snail venom, known as ω-conotoxin MVIIA (Ziconotide), specifically binds to N-type calcium channels and inhibits their activity, making it a potent analgesic for treating chronic pain.

T-type calcium channels are a type of voltage-gated calcium channel that play a role in the regulation of excitable cells, such as neurons and cardiac myocytes. These channels are characterized by their low voltage activation threshold and rapid activation and inactivation kinetics. They are involved in various physiological processes, including neuronal excitability, gene expression, hormone secretion, and heart rhythm. Abnormal functioning of T-type calcium channels has been implicated in several diseases, such as epilepsy, chronic pain, and cardiac arrhythmias.

Calcium signaling is the process by which cells regulate various functions through changes in intracellular calcium ion concentrations. Calcium ions (Ca^2+^) are crucial second messengers that play a critical role in many cellular processes, including muscle contraction, neurotransmitter release, gene expression, and programmed cell death (apoptosis).

Intracellular calcium levels are tightly regulated by a complex network of channels, pumps, and exchangers located on the plasma membrane and intracellular organelles such as the endoplasmic reticulum (ER) and mitochondria. These proteins control the influx, efflux, and storage of calcium ions within the cell.

Calcium signaling is initiated when an external signal, such as a hormone or neurotransmitter, binds to a specific receptor on the plasma membrane. This interaction triggers the opening of ion channels, allowing extracellular Ca^2+^ to flow into the cytoplasm. In some cases, this influx of calcium ions is sufficient to activate downstream targets directly. However, in most instances, the increase in intracellular Ca^2+^ serves as a trigger for the release of additional calcium from internal stores, such as the ER.

The release of calcium from the ER is mediated by ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP3Rs), which are activated by specific second messengers generated in response to the initial external signal. The activation of these channels leads to a rapid increase in cytoplasmic Ca^2+^, creating a transient intracellular calcium signal known as a "calcium spark" or "calcium puff."

These localized increases in calcium concentration can then propagate throughout the cell as waves of elevated calcium, allowing for the spatial and temporal coordination of various cellular responses. The duration and amplitude of these calcium signals are finely tuned by the interplay between calcium-binding proteins, pumps, and exchangers, ensuring that appropriate responses are elicited in a controlled manner.

Dysregulation of intracellular calcium signaling has been implicated in numerous pathological conditions, including neurodegenerative diseases, cardiovascular disorders, and cancer. Therefore, understanding the molecular mechanisms governing calcium homeostasis and signaling is crucial for the development of novel therapeutic strategies targeting these diseases.

Ion channel gating refers to the process by which ion channels in cell membranes open and close in response to various stimuli, allowing ions such as sodium, potassium, and calcium to flow into or out of the cell. This movement of ions is crucial for many physiological processes, including the generation and transmission of electrical signals in nerve cells, muscle contraction, and the regulation of hormone secretion.

Ion channel gating can be regulated by various factors, including voltage changes across the membrane (voltage-gated channels), ligand binding (ligand-gated channels), mechanical stress (mechanosensitive channels), or other intracellular signals (second messenger-gated channels). The opening and closing of ion channels are highly regulated and coordinated processes that play a critical role in maintaining the proper functioning of cells and organ systems.

Voltage-gated sodium channel agonists are substances that enhance the activity or increase the opening frequency of voltage-gated sodium channels. These channels play a crucial role in the initiation and propagation of action potentials in excitable cells, such as neurons and muscle fibers. By increasing the likelihood of sodium ion influx into the cell, agonists can cause hyperexcitability, leading to various physiological effects, including the generation of pain signals or muscle contraction.

It is important to note that voltage-gated sodium channel agonists are not commonly used in a therapeutic context due to their potential to induce abnormal excitability and associated adverse effects. Instead, antagonists (blockers) of these channels are often employed to treat conditions like neuropathic pain or epilepsy, where reducing neuronal hyperexcitability is desirable.

Potassium channel blockers are a class of medications that work by blocking potassium channels, which are proteins in the cell membrane that control the movement of potassium ions into and out of cells. By blocking these channels, potassium channel blockers can help to regulate electrical activity in the heart, making them useful for treating certain types of cardiac arrhythmias (irregular heart rhythms).

There are several different types of potassium channel blockers, including:

1. Class III antiarrhythmic drugs: These medications, such as amiodarone and sotalol, are used to treat and prevent serious ventricular arrhythmias (irregular heart rhythms that originate in the lower chambers of the heart).
2. Calcium channel blockers: While not strictly potassium channel blockers, some calcium channel blockers also have effects on potassium channels. These medications, such as diltiazem and verapamil, are used to treat hypertension (high blood pressure), angina (chest pain), and certain types of arrhythmias.
3. Non-selective potassium channel blockers: These medications, such as 4-aminopyridine and tetraethylammonium, have a broader effect on potassium channels and are used primarily in research settings to study the electrical properties of cells.

It's important to note that potassium channel blockers can have serious side effects, particularly when used in high doses or in combination with other medications that affect heart rhythms. They should only be prescribed by a healthcare provider who is familiar with their use and potential risks.

ATP-sensitive potassium (KATP) channels are a type of ion channel found in the membranes of cells, including those in the heart, muscle, and pancreas. These channels are unique because their opening and closing are regulated by the levels of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) in the cell.

Under normal conditions, when ATP levels are high and ADP levels are low, the KATP channels are closed, which allows the cells to maintain their normal electrical activity. However, during times of metabolic stress or ischemia (a lack of blood flow), the levels of ATP in the cell decrease while the levels of ADP increase. This change in the ATP-to-ADP ratio causes the KATP channels to open, which allows potassium ions to flow out of the cell. The efflux of potassium ions then leads to hyperpolarization of the cell membrane, which helps to protect the cells from damage.

In the pancreas, KATP channels play a crucial role in regulating insulin secretion. In the beta cells of the pancreas, an increase in blood glucose levels leads to an increase in ATP production and a decrease in ADP levels, which causes the KATP channels to close. This closure of the KATP channels leads to depolarization of the cell membrane, which triggers the release of insulin.

Overall, KATP channels are important regulators of cellular electrical activity and play a critical role in protecting cells from damage during times of metabolic stress or ischemia.

Diltiazem is a calcium channel blocker medication that is used to treat hypertension (high blood pressure), angina (chest pain), and certain heart rhythm disorders. It works by relaxing the muscles of the blood vessels, which lowers blood pressure and improves blood flow to the heart. Diltiazem may also be used to reduce the risk of heart attack in patients with coronary artery disease.

The medication is available in various forms, including immediate-release tablets, extended-release tablets, and extended-release capsules. It is usually taken orally, one to three times a day, depending on the formulation and the individual patient's needs. Diltiazem may cause side effects such as dizziness, headache, nausea, and constipation.

It is important to follow the dosage instructions provided by your healthcare provider and to inform them of any other medications you are taking, as well as any medical conditions you have, before starting diltiazem.

Inwardly rectifying potassium channels (Kir) are a type of potassium channel that allow for the selective passage of potassium ions (K+) across cell membranes. The term "inwardly rectifying" refers to their unique property of allowing potassium ions to flow more easily into the cell (inward current) than out of the cell (outward current). This characteristic is due to the voltage-dependent blockage of these channels by intracellular magnesium and polyamines at depolarized potentials.

These channels play crucial roles in various physiological processes, including:

1. Resting membrane potential maintenance: Kir channels help establish and maintain the negative resting membrane potential in cells by facilitating potassium efflux when the membrane potential is near the potassium equilibrium potential (Ek).
2. Action potential repolarization: In excitable cells like neurons and muscle fibers, Kir channels contribute to the rapid repolarization phase of action potentials, allowing for proper electrical signaling.
3. Cell volume regulation: Kir channels are involved in regulating cell volume by mediating potassium influx during osmotic stress or changes in intracellular ion concentrations.
4. Insulin secretion: In pancreatic β-cells, Kir channels control the membrane potential and calcium signaling necessary for insulin release.
5. Renal function: Kir channels are essential for maintaining electrolyte balance and controlling renal tubular transport in the kidneys.

There are several subfamilies of inwardly rectifying potassium channels (Kir1-7), each with distinct biophysical properties, tissue distributions, and functions. Mutations in genes encoding these channels can lead to various human diseases, including cardiac arrhythmias, epilepsy, and Bartter syndrome.

Calcium channels, P-type, are a specific type of voltage-gated calcium channel found in excitable cells such as neurons and muscle cells. They are named "P-type" because they were initially identified in Purkinje cells of the cerebellum. These channels play a crucial role in various cellular processes, including neurotransmitter release, muscle contraction, and gene expression.

P-type calcium channels are characterized by their unique biophysical properties, such as slow voltage-dependent activation and inactivation, as well as sensitivity to the drug felodipine. They are composed of several subunits, including the pore-forming α1 subunit, which contains the voltage sensor and the selectivity filter for calcium ions. The α1 subunit is associated with accessory subunits, such as β, γ, and δ, that modulate the channel's properties and trafficking to the cell membrane.

P-type calcium channels are important targets for therapeutic interventions in various diseases, including neurological disorders, cardiovascular diseases, and cancer. For example, drugs that block P-type calcium channels have been used to treat hypertension and angina, while activators of these channels have shown promise in treating neurodegenerative disorders such as Parkinson's disease.

Calcium channels, Q-type, are a type of voltage-gated calcium channel found in various tissues, including the brain and heart. They are called "Q-type" because they exhibit a distinctive "q-wave" in their current trace during electrical activity. These channels play important roles in regulating physiological processes such as neurotransmitter release, hormone secretion, and cardiac muscle contraction.

The pore-forming subunit of Q-type calcium channels is the CaV2.1 (or α1A) subunit, which is encoded by the CACNA1A gene. These channels are activated by depolarization of the cell membrane and allow the influx of calcium ions into the cell. The resulting increase in intracellular calcium concentration triggers various downstream signaling pathways that mediate the physiological responses mentioned above.

Dysfunction of Q-type calcium channels has been implicated in several neurological and cardiovascular disorders, including migraine, epilepsy, cerebellar ataxia, and hypertension. Therefore, understanding the structure, function, and regulation of these channels is an important area of research for developing new therapeutic strategies to treat these conditions.

Electrophysiology is a branch of medicine that deals with the electrical activities of the body, particularly the heart. In a medical context, electrophysiology studies (EPS) are performed to assess abnormal heart rhythms (arrhythmias) and to evaluate the effectiveness of certain treatments, such as medication or pacemakers.

During an EPS, electrode catheters are inserted into the heart through blood vessels in the groin or neck. These catheters can record the electrical activity of the heart and stimulate it to help identify the source of the arrhythmia. The information gathered during the study can help doctors determine the best course of treatment for each patient.

In addition to cardiac electrophysiology, there are also other subspecialties within electrophysiology, such as neuromuscular electrophysiology, which deals with the electrical activity of the nervous system and muscles.

Nimodipine is an antihypertensive and calcium channel blocker drug, which is primarily used in the prevention and treatment of neurological deficits following subarachnoid hemorrhage (SAH), a type of stroke caused by bleeding in the space surrounding the brain. It works by relaxing and dilating blood vessels in the brain, improving blood flow, and preventing spasms in cerebral arteries, which can help reduce the risk of further damage to brain tissues.

Nimodipine is available in the form of capsules or an injectable solution for medical use. It is crucial to follow a healthcare professional's instructions carefully when using this medication, as improper usage may lead to unwanted side effects or reduced effectiveness. Common side effects include headache, dizziness, nausea, and flushing.

It is essential to consult with a healthcare provider for personalized medical advice regarding the use of Nimodipine or any other medications.

Verapamil is a calcium channel blocker medication that is primarily used to treat hypertension (high blood pressure), angina (chest pain), and certain types of cardiac arrhythmias (irregular heart rhyats). It works by relaxing the smooth muscle cells in the walls of blood vessels, which causes them to dilate or widen, reducing the resistance to blood flow and thereby lowering blood pressure. Verapamil also slows down the conduction of electrical signals within the heart, which can help to regulate the heart rate and rhythm.

In addition to its cardiovascular effects, verapamil is sometimes used off-label for the treatment of other conditions such as migraine headaches, Raynaud's phenomenon, and certain types of tremors. It is available in various forms, including immediate-release tablets, extended-release capsules, and intravenous (IV) injection.

It is important to note that verapamil can interact with other medications, so it is essential to inform your healthcare provider about all the drugs you are taking before starting this medication. Additionally, verapamil should be used with caution in people with certain medical conditions, such as heart failure, liver disease, and low blood pressure.

Membrane potential is the electrical potential difference across a cell membrane, typically for excitable cells such as nerve and muscle cells. It is the difference in electric charge between the inside and outside of a cell, created by the selective permeability of the cell membrane to different ions. The resting membrane potential of a typical animal cell is around -70 mV, with the interior being negative relative to the exterior. This potential is generated and maintained by the active transport of ions across the membrane, primarily through the action of the sodium-potassium pump. Membrane potentials play a crucial role in many physiological processes, including the transmission of nerve impulses and the contraction of muscle cells.

R-type calcium channels are a type of voltage-gated calcium channel found in excitable cells such as neurons and muscle cells. They are named "R" for "resistant," because they are less sensitive to blockers that inhibit other types of calcium channels. R-type calcium channels play important roles in various physiological processes, including regulation of neurotransmitter release, excitation-contraction coupling in muscle cells, and gene expression. They are composed of several subunits, including the pore-forming α1E subunit, which determines the channel's electrophysiological properties, and accessory subunits that modulate the channel's function. R-type calcium channels are activated by depolarization of the cell membrane and allow the influx of calcium ions into the cell, which can trigger various downstream signaling pathways.

Patch-clamp techniques are a group of electrophysiological methods used to study ion channels and other electrical properties of cells. These techniques were developed by Erwin Neher and Bert Sakmann, who were awarded the Nobel Prize in Physiology or Medicine in 1991 for their work. The basic principle of patch-clamp techniques involves creating a high resistance seal between a glass micropipette and the cell membrane, allowing for the measurement of current flowing through individual ion channels or groups of channels.

There are several different configurations of patch-clamp techniques, including:

1. Cell-attached configuration: In this configuration, the micropipette is attached to the outer surface of the cell membrane, and the current flowing across a single ion channel can be measured. This configuration allows for the study of the properties of individual channels in their native environment.
2. Whole-cell configuration: Here, the micropipette breaks through the cell membrane, creating a low resistance electrical connection between the pipette and the inside of the cell. This configuration allows for the measurement of the total current flowing across all ion channels in the cell membrane.
3. Inside-out configuration: In this configuration, the micropipette is pulled away from the cell after establishing a seal, resulting in the exposure of the inner surface of the cell membrane to the solution in the pipette. This configuration allows for the study of the properties of ion channels in isolation from other cellular components.
4. Outside-out configuration: Here, the micropipette is pulled away from the cell after establishing a seal, resulting in the exposure of the outer surface of the cell membrane to the solution in the pipette. This configuration allows for the study of the properties of ion channels in their native environment, but with the ability to control the composition of the extracellular solution.

Patch-clamp techniques have been instrumental in advancing our understanding of ion channel function and have contributed to numerous breakthroughs in neuroscience, pharmacology, and physiology.

Chloride channels are membrane proteins that form hydrophilic pores or gaps, allowing the selective passage of chloride ions (Cl-) across the lipid bilayer of cell membranes. They play crucial roles in various physiological processes, including regulation of neuronal excitability, maintenance of resting membrane potential, fluid and electrolyte transport, and pH and volume regulation of cells.

Chloride channels can be categorized into several groups based on their structure, function, and mechanism of activation. Some of the major classes include:

1. Voltage-gated chloride channels (ClC): These channels are activated by changes in membrane potential and have a variety of functions, such as regulating neuronal excitability and transepithelial transport.
2. Ligand-gated chloride channels: These channels are activated by the binding of specific ligands or messenger molecules, like GABA (gamma-aminobutyric acid) or glycine, and are involved in neurotransmission and neuromodulation.
3. Cystic fibrosis transmembrane conductance regulator (CFTR): This is a chloride channel primarily located in the apical membrane of epithelial cells, responsible for secreting chloride ions and water to maintain proper hydration and mucociliary clearance in various organs, including the lungs and pancreas.
4. Calcium-activated chloride channels (CaCCs): These channels are activated by increased intracellular calcium concentrations and participate in various physiological processes, such as smooth muscle contraction, neurotransmitter release, and cell volume regulation.
5. Swelling-activated chloride channels (ClSwells): Also known as volume-regulated anion channels (VRACs), these channels are activated by cell swelling or osmotic stress and help regulate cell volume and ionic homeostasis.

Dysfunction of chloride channels has been implicated in various human diseases, such as cystic fibrosis, myotonia congenita, epilepsy, and certain forms of cancer.

Pinacidil is not typically defined in a medical dictionary as it is a specific pharmaceutical compound, rather than a general medical term. However, I can provide you with information about what Pinacidil is.

Pinacidil is an oral antihypertensive medication that acts as a direct activator of ATP-sensitive potassium (KATP) channels. These channels are present in various tissues, including the pancreas, heart, and smooth muscle cells. By opening KATP channels, Pinacidil causes hyperpolarization of the cell membrane, which leads to relaxation of smooth muscles in blood vessels. This results in vasodilation and a decrease in blood pressure.

Pinacidil is used off-label for the treatment of pulmonary arterial hypertension (PAH) due to its ability to dilate pulmonary arteries. However, it is not commonly prescribed for this purpose due to the availability of other FDA-approved medications specifically designed for PAH treatment.

Please consult a healthcare professional or pharmacist for more detailed information about Pinacidil and its uses, side effects, and potential interactions with other medications.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Barium is a naturally occurring, silvery-white metallic chemical element with the symbol Ba and atomic number 56. In medical terms, barium is commonly used as a contrast agent in radiology, particularly in X-ray examinations such as an upper GI series or barium enema. The barium sulfate powder is mixed with water to create a liquid or thick paste that is swallowed or inserted through the rectum. This provides a white coating on the inside lining of the digestive tract, allowing it to be seen more clearly on X-ray images and helping doctors diagnose various conditions such as ulcers, tumors, or inflammation.

It's important to note that barium is not absorbed by the body and does not cause any harm when used in medical imaging procedures. However, if it is accidentally inhaled or aspirated into the lungs during administration, it can cause chemical pneumonitis, a potentially serious condition. Therefore, it should only be administered under the supervision of trained medical professionals.

Omega-Conotoxin GVIA is a specific type of conotoxin, a peptide toxin derived from the venom of marine cone snails. This particular variant comes from the Conus geographus species.

Omega-Conotoxins are known for their ability to block N-type voltage-gated calcium channels (VGCCs). In the case of omega-Conotoxin GVIA, it specifically and potently inhibits N-type VGCCs, which play crucial roles in neurotransmitter release and pain signaling. Therefore, it has been extensively studied as a research tool to understand these channels' functions and as a potential lead compound for developing novel therapeutics, particularly for treating chronic pain conditions.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Electric conductivity, also known as electrical conductance, is a measure of a material's ability to allow the flow of electric current through it. It is usually measured in units of Siemens per meter (S/m) or ohm-meters (Ω-m).

In medical terms, electric conductivity can refer to the body's ability to conduct electrical signals, which is important for various physiological processes such as nerve impulse transmission and muscle contraction. Abnormalities in electrical conductivity can be associated with various medical conditions, including neurological disorders and heart diseases.

For example, in electrocardiography (ECG), the electric conductivity of the heart is measured to assess its electrical activity and identify any abnormalities that may indicate heart disease. Similarly, in electromyography (EMG), the electric conductivity of muscles is measured to diagnose neuromuscular disorders.

Dietary calcium is a type of calcium that is obtained through food sources. Calcium is an essential mineral that is necessary for many bodily functions, including bone formation and maintenance, muscle contraction, nerve impulse transmission, and blood clotting.

The recommended daily intake of dietary calcium varies depending on age, sex, and other factors. For example, the recommended daily intake for adults aged 19-50 is 1000 mg, while women over 50 and men over 70 require 1200 mg per day.

Good dietary sources of calcium include dairy products such as milk, cheese, and yogurt; leafy green vegetables like broccoli and kale; fortified cereals and juices; and certain types of fish, such as salmon and sardines. It is important to note that some foods can inhibit the absorption of calcium, including oxalates found in spinach and rhubarb, and phytates found in whole grains and legumes.

If a person is unable to get enough calcium through their diet, they may need to take calcium supplements. However, it is important to talk to a healthcare provider before starting any new supplement regimen, as excessive intake of calcium can lead to negative health effects.

In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."

1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.

2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.

3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.

4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).

Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.

Epithelial Sodium Channel (ENaC) Agonists are substances that increase the activity or expression of ENaC, which are ion channels present in the epithelial cells of various organs including the lungs, kidneys, and colon. These channels play a crucial role in regulating sodium and fluid balance in the body.

ENaC agonists can enhance sodium absorption across epithelial surfaces, leading to an increase in extracellular fluid volume and blood pressure. They have been studied as potential therapeutic agents for conditions associated with excessive fluid loss, such as diarrhea or respiratory distress syndrome. However, their use is limited due to the risk of adverse effects, including increased blood pressure and potential heart problems.

Examples of ENaC agonists include certain steroid hormones like aldosterone, as well as synthetic compounds such as benzamil and amiloride. It's important to note that while these substances can act as ENaC agonists, they may also have other effects on various biological systems, and their use should be carefully monitored by healthcare professionals.

Omega-conotoxins are a group of peptides found in the venom of cone snails. They are characterized by their ability to block N-type voltage-gated calcium channels ( CaV2.2) in the nervous system. These toxins play a crucial role in the predatory behavior of cone snails, as they help to immobilize prey by inhibiting neurotransmitter release. In medical research, omega-conotoxins are used as tools to study neuronal function and are also being investigated for their potential therapeutic applications, particularly in the treatment of chronic pain.

Neurons, also known as nerve cells or neurocytes, are specialized cells that constitute the basic unit of the nervous system. They are responsible for receiving, processing, and transmitting information and signals within the body. Neurons have three main parts: the dendrites, the cell body (soma), and the axon. The dendrites receive signals from other neurons or sensory receptors, while the axon transmits these signals to other neurons, muscles, or glands. The junction between two neurons is called a synapse, where neurotransmitters are released to transmit the signal across the gap (synaptic cleft) to the next neuron. Neurons vary in size, shape, and structure depending on their function and location within the nervous system.

Voltage-gated potassium channels are a type of ion channel found in the membrane of excitable cells such as nerve and muscle cells. They are called "voltage-gated" because their opening and closing is regulated by the voltage, or electrical potential, across the cell membrane. Specifically, these channels are activated when the membrane potential becomes more positive, a condition that occurs during the action potential of a neuron or muscle fiber.

When voltage-gated potassium channels open, they allow potassium ions (K+) to flow out of the cell down their electrochemical gradient. This outward flow of K+ ions helps to repolarize the membrane, bringing it back to its resting potential after an action potential has occurred. The precise timing and duration of the opening and closing of voltage-gated potassium channels is critical for the normal functioning of excitable cells, and abnormalities in these channels have been linked to a variety of diseases, including cardiac arrhythmias, epilepsy, and neurological disorders.

Potassium is a essential mineral and an important electrolyte that is widely distributed in the human body. The majority of potassium in the body (approximately 98%) is found within cells, with the remaining 2% present in blood serum and other bodily fluids. Potassium plays a crucial role in various physiological processes, including:

1. Regulation of fluid balance and maintenance of normal blood pressure through its effects on vascular tone and sodium excretion.
2. Facilitation of nerve impulse transmission and muscle contraction by participating in the generation and propagation of action potentials.
3. Protein synthesis, enzyme activation, and glycogen metabolism.
4. Regulation of acid-base balance through its role in buffering systems.

The normal serum potassium concentration ranges from 3.5 to 5.0 mEq/L (milliequivalents per liter) or mmol/L (millimoles per liter). Potassium levels outside this range can have significant clinical consequences, with both hypokalemia (low potassium levels) and hyperkalemia (high potassium levels) potentially leading to serious complications such as cardiac arrhythmias, muscle weakness, and respiratory failure.

Potassium is primarily obtained through the diet, with rich sources including fruits (e.g., bananas, oranges, and apricots), vegetables (e.g., leafy greens, potatoes, and tomatoes), legumes, nuts, dairy products, and meat. In cases of deficiency or increased needs, potassium supplements may be recommended under the guidance of a healthcare professional.

Calcium-activated potassium channels are a type of ion channel found in the membranes of cells. These channels are activated by an increase in intracellular calcium levels and play a crucial role in regulating various cellular processes, including electrical excitability, neurotransmitter release, hormone secretion, and vascular tone.

Once activated, calcium-activated potassium channels allow potassium ions (K+) to flow out of the cell, which can lead to membrane hyperpolarization or stabilization of the resting membrane potential. This process helps control the frequency and duration of action potentials in excitable cells such as neurons and muscle fibers.

There are several subtypes of calcium-activated potassium channels, including:

1. Large conductance calcium-activated potassium (BK) channels: These channels have a large single-channel conductance and are activated by both voltage and intracellular calcium. They play essential roles in regulating vascular tone, neurotransmitter release, and neuronal excitability.
2. Small conductance calcium-activated potassium (SK) channels: These channels have a smaller single-channel conductance and are primarily activated by intracellular calcium. They contribute to the regulation of neuronal excitability and neurotransmitter release.
3. Intermediate conductance calcium-activated potassium (IK) channels: These channels have an intermediate single-channel conductance and are activated by both voltage and intracellular calcium. They play a role in regulating epithelial ion transport, smooth muscle cell excitability, and neurotransmitter release.

Dysfunction of calcium-activated potassium channels has been implicated in various pathological conditions, such as hypertension, epilepsy, chronic pain, and neurological disorders.

Glyburide is a medication that falls under the class of drugs known as sulfonylureas. It is primarily used to manage type 2 diabetes by lowering blood sugar levels. Glyburide works by stimulating the release of insulin from the pancreas, thereby increasing the amount of insulin available in the body to help glucose enter cells and decrease the level of glucose in the bloodstream.

The medical definition of Glyburide is:
A second-generation sulfonylurea antidiabetic drug (oral hypoglycemic) used in the management of type 2 diabetes mellitus. It acts by stimulating pancreatic beta cells to release insulin and increases peripheral glucose uptake and utilization, thereby reducing blood glucose levels. Glyburide may also decrease glucose production in the liver.

It is important to note that Glyburide should be used as part of a comprehensive diabetes management plan that includes proper diet, exercise, regular monitoring of blood sugar levels, and other necessary lifestyle modifications. As with any medication, it can have side effects and potential interactions with other drugs, so it should only be taken under the supervision of a healthcare provider.

An action potential is a brief electrical signal that travels along the membrane of a nerve cell (neuron) or muscle cell. It is initiated by a rapid, localized change in the permeability of the cell membrane to specific ions, such as sodium and potassium, resulting in a rapid influx of sodium ions and a subsequent efflux of potassium ions. This ion movement causes a brief reversal of the electrical potential across the membrane, which is known as depolarization. The action potential then propagates along the cell membrane as a wave, allowing the electrical signal to be transmitted over long distances within the body. Action potentials play a crucial role in the communication and functioning of the nervous system and muscle tissue.

Nicorandil is a medication that belongs to a class of drugs known as potassium channel activators. It works by relaxing and widening blood vessels, which improves blood flow and reduces the workload on the heart. Nicorandil is primarily used to treat chronic stable angina, a type of chest pain caused by reduced blood flow to the heart muscle.

The medical definition of Nicorandil can be described as:

A synthetic derivative of nicotinamide with vasodilatory properties, acting as an opener of ATP-sensitive potassium channels in vascular smooth muscle and cardiomyocytes. It is used in the management of chronic stable angina, providing both antianginal and antiischemic effects through a dual mechanism that includes coronary and peripheral vasodilation. By reducing afterload and preload, Nicorandil decreases myocardial oxygen demand while increasing supply, leading to improved exercise tolerance and reduced frequency of anginal episodes.

Cromakalim is a pharmacological agent, specifically a potassium channel opener, that was investigated for its potential therapeutic effects in the treatment of cardiovascular diseases such as hypertension and angina. Potassium channel openers work by relaxing smooth muscle cells in blood vessels, which leads to vasodilation and decreased blood pressure. However, cromakalim was never approved for clinical use due to its associated side effects, including negative inotropic effects on the heart and potential proarrhythmic properties.

Mibefradil is a medication that was previously used to treat hypertension (high blood pressure) and angina (chest pain due to reduced blood flow to the heart muscle). It belongs to a class of drugs known as calcium channel blockers, which work by relaxing the muscles of the blood vessels and increasing the supply of blood and oxygen to the heart while reducing its workload.

Mibefradil was first approved for medical use in 1997 but was later withdrawn from the market in 1998 due to its interactions with several other medications, which could lead to dangerous side effects. Currently, it is not available for medical use.

Sodium channel blockers are a class of medications that work by blocking sodium channels in the heart, which prevents the rapid influx of sodium ions into the cells during depolarization. This action slows down the rate of impulse generation and propagation in the heart, which in turn decreases the heart rate and prolongs the refractory period.

Sodium channel blockers are primarily used to treat cardiac arrhythmias, including atrial fibrillation, atrial flutter, and ventricular tachycardia. They may also be used to treat certain types of neuropathic pain. Examples of sodium channel blockers include Class I antiarrhythmics such as flecainide, propafenone, lidocaine, and mexiletine.

It's important to note that sodium channel blockers can have potential side effects, including proarrhythmia (i.e., the development of new arrhythmias or worsening of existing ones), negative inotropy (decreased contractility of the heart muscle), and cardiac conduction abnormalities. Therefore, these medications should be used with caution and under the close supervision of a healthcare provider.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

The myocardium is the middle layer of the heart wall, composed of specialized cardiac muscle cells that are responsible for pumping blood throughout the body. It forms the thickest part of the heart wall and is divided into two sections: the left ventricle, which pumps oxygenated blood to the rest of the body, and the right ventricle, which pumps deoxygenated blood to the lungs.

The myocardium contains several types of cells, including cardiac muscle fibers, connective tissue, nerves, and blood vessels. The muscle fibers are arranged in a highly organized pattern that allows them to contract in a coordinated manner, generating the force necessary to pump blood through the heart and circulatory system.

Damage to the myocardium can occur due to various factors such as ischemia (reduced blood flow), infection, inflammation, or genetic disorders. This damage can lead to several cardiac conditions, including heart failure, arrhythmias, and cardiomyopathy.

Lambert-Eaton Myasthenic Syndrome (LEMS) is a rare autoimmune disorder characterized by muscle weakness and fatigability. It is caused by the presence of antibodies against voltage-gated calcium channels (VGCC) in the neuromuscular junction, which disrupts the normal transmission of signals between nerves and muscles.

The symptoms of LEMS include proximal muscle weakness, which may affect the legs more than the arms, and autonomic dysfunction such as dry mouth and constipation. The weakness tends to improve with exercise but worsens after periods of rest. In some cases, LEMS can be associated with cancer, particularly small cell lung cancer.

Diagnosis of LEMS typically involves a combination of clinical evaluation, electromyography (EMG) studies, and blood tests to detect VGCC antibodies. Treatment may include medications such as pyridostigmine, which improves neuromuscular transmission, or intravenous immunoglobulin and plasma exchange, which help to reduce the immune response. In cases where LEMS is associated with cancer, treatment of the underlying malignancy can also improve muscle strength and function.

"Pyrroles" is not a medical term in and of itself, but "pyrrole" is an organic compound that contains one nitrogen atom and four carbon atoms in a ring structure. In the context of human health, "pyrroles" often refers to a group of compounds called pyrrol derivatives or pyrrole metabolites.

In clinical settings, "pyrroles" is sometimes used to refer to a urinary metabolite called "pyrrole-protein conjugate," which contains a pyrrole ring and is excreted in the urine. Elevated levels of this compound have been associated with certain psychiatric and behavioral disorders, such as schizophrenia and mood disorders. However, the relationship between pyrroles and these conditions is not well understood, and more research is needed to establish a clear medical definition or diagnostic criteria for "pyrrole disorder" or "pyroluria."

Transient Receptor Potential Canonical (TRPC) cation channels are a subfamily of the TRP superfamily of non-selective cation channels. They are widely expressed in various tissues and play crucial roles in many cellular processes, including sensory perception, cell proliferation, and migration. TRPC channels are permeable to both monovalent (sodium and potassium) and divalent (calcium and magnesium) cations, and their activation can lead to a rise in intracellular calcium concentration, which in turn regulates various downstream signaling pathways. TRPC channels can be activated by a variety of stimuli, including G protein-coupled receptors, receptor tyrosine kinases, and mechanical stress. Mutations in TRPC genes have been associated with several human diseases, including hereditary hearing loss, cardiovascular disorders, and neurological conditions.

Omega-Agatoxin IVA is a specific type of neurotoxin that is derived from the venom of the funnel web spider, Agelenopsis aperta. It is known to selectively target and block P/Q-type voltage-gated calcium channels, which are found in the presynaptic terminals of neurons. These channels play a crucial role in the release of neurotransmitters, the chemical signals that neurons use to communicate with each other.

By blocking these channels, omega-Agatoxin IVA can prevent the release of neurotransmitters and interfere with the normal functioning of the nervous system. It is a valuable tool in neuroscience research for studying the role of calcium channels in various physiological processes and has been used to investigate conditions such as pain, epilepsy, and neurological disorders.

It's important to note that while omega-Agatoxin IVA has potential therapeutic applications, it is primarily used for research purposes and should be handled with care due to its potent neurotoxic effects.

Veratridine is not a medical term, but it is a chemical compound that has been used in scientific research. It's a plant alkaloid found primarily in the seeds and roots of various Veratrum species (also known as false hellebore or white hellebore).

In a pharmacological context, veratridine can be defined as:

A steroidal alkaloid that acts as a potent agonist at voltage-gated sodium channels in excitable membranes. It causes persistent activation of these channels, leading to sustained depolarization and increased neuronal excitability. Veratridine has been used in research to study the properties and functions of sodium channels, as well as neurotransmission and nerve impulse transmission.

However, it is not a term typically used in clinical medicine or patient care.

The Shaker superfamily of potassium channels, also known as Kv channels (voltage-gated potassium channels), refers to a group of ion channels that are responsible for the selective transport of potassium ions across the cell membrane. These channels are crucial for regulating the electrical excitability of cells, particularly in neurons and muscle cells.

The Shaker superfamily is named after the Drosophila melanogaster (fruit fly) gene shaker, which was the first voltage-gated potassium channel to be identified and cloned. The channels in this family share a common structure, consisting of four subunits that each contain six transmembrane domains. The fourth domain contains the voltage sensor, which responds to changes in membrane potential and triggers the opening or closing of the channel pore.

The Shaker superfamily is further divided into several subfamilies based on their sequence similarity and functional properties. These include the Shaw, Shab, and Shal subfamilies, among others. Each subfamily has distinct biophysical and pharmacological properties that allow for selective activation or inhibition by various drugs and toxins.

Overall, the Shaker superfamily of potassium channels plays a critical role in maintaining the electrical excitability of cells and is involved in a wide range of physiological processes, including nerve impulse transmission, muscle contraction, and hormone secretion.

I believe there may be some confusion in your question. "Rabbits" is a common name used to refer to the Lagomorpha species, particularly members of the family Leporidae. They are small mammals known for their long ears, strong legs, and quick reproduction.

However, if you're referring to "rabbits" in a medical context, there is a term called "rabbit syndrome," which is a rare movement disorder characterized by repetitive, involuntary movements of the fingers, resembling those of a rabbit chewing. It is also known as "finger-chewing chorea." This condition is usually associated with certain medications, particularly antipsychotics, and typically resolves when the medication is stopped or adjusted.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Dopamine agonists are a class of medications that mimic the action of dopamine, a neurotransmitter in the brain that regulates movement, emotion, motivation, and reinforcement of rewarding behaviors. These medications bind to dopamine receptors in the brain and activate them, leading to an increase in dopaminergic activity.

Dopamine agonists are used primarily to treat Parkinson's disease, a neurological disorder characterized by motor symptoms such as tremors, rigidity, bradykinesia (slowness of movement), and postural instability. By increasing dopaminergic activity in the brain, dopamine agonists can help alleviate some of these symptoms.

Examples of dopamine agonists include:

1. Pramipexole (Mirapex)
2. Ropinirole (Requip)
3. Rotigotine (Neupro)
4. Apomorphine (Apokyn)

Dopamine agonists may also be used off-label to treat other conditions, such as restless legs syndrome or certain types of dopamine-responsive dystonia. However, these medications can have significant side effects, including nausea, dizziness, orthostatic hypotension, compulsive behaviors (such as gambling, shopping, or sexual addiction), and hallucinations. Therefore, they should be used with caution and under the close supervision of a healthcare provider.

Potassium chloride is an essential electrolyte that is often used in medical settings as a medication. It's a white, crystalline salt that is highly soluble in water and has a salty taste. In the body, potassium chloride plays a crucial role in maintaining fluid and electrolyte balance, nerve function, and muscle contraction.

Medically, potassium chloride is commonly used to treat or prevent low potassium levels (hypokalemia) in the blood. Hypokalemia can occur due to various reasons such as certain medications, kidney diseases, vomiting, diarrhea, or excessive sweating. Potassium chloride is available in various forms, including tablets, capsules, and liquids, and it's usually taken by mouth.

It's important to note that potassium chloride should be used with caution and under the supervision of a healthcare provider, as high levels of potassium (hyperkalemia) can be harmful and even life-threatening. Hyperkalemia can cause symptoms such as muscle weakness, irregular heartbeat, and cardiac arrest.

In medical terms, the heart is a muscular organ located in the thoracic cavity that functions as a pump to circulate blood throughout the body. It's responsible for delivering oxygen and nutrients to the tissues and removing carbon dioxide and other wastes. The human heart is divided into four chambers: two atria on the top and two ventricles on the bottom. The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs, while the left side receives oxygenated blood from the lungs and pumps it out to the rest of the body. The heart's rhythmic contractions and relaxations are regulated by a complex electrical conduction system.

Adenosine Triphosphate (ATP) is a high-energy molecule that stores and transports energy within cells. It is the main source of energy for most cellular processes, including muscle contraction, nerve impulse transmission, and protein synthesis. ATP is composed of a base (adenine), a sugar (ribose), and three phosphate groups. The bonds between these phosphate groups contain a significant amount of energy, which can be released when the bond between the second and third phosphate group is broken, resulting in the formation of adenosine diphosphate (ADP) and inorganic phosphate. This process is known as hydrolysis and can be catalyzed by various enzymes to drive a wide range of cellular functions. ATP can also be regenerated from ADP through various metabolic pathways, such as oxidative phosphorylation or substrate-level phosphorylation, allowing for the continuous supply of energy to cells.

Large-conductance calcium-activated potassium channels (BK channels) are a type of ion channel found in the membranes of many types of cells, including excitable cells such as neurons and muscle cells. These channels are characterized by their large conductance to potassium ions (K+), which allows them to significantly impact the electrical excitability of cells.

BK channels are activated by both voltage and intracellular calcium ions (Ca2+). They are therefore also known as Ca2+-activated K+ (KCa) channels. When the membrane potential becomes more positive (depolarized), and/or when intracellular Ca2+ levels rise, BK channels open, allowing K+ to flow out of the cell. This efflux of K+ tends to hyperpolarize the membrane potential, making it more difficult for the cell to generate further action potentials or contractile responses.

BK channels play important roles in regulating a variety of physiological processes, including neuronal excitability, neurotransmitter release, vascular tone, and cardiac electrical activity. Dysfunction of BK channels has been implicated in several diseases, such as hypertension, epilepsy, and chronic pain.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

Benzopyrans are a class of chemical compounds that contain a benzene ring fused to a pyran ring. They are also known as chromenes. Benzopyrans can be found in various natural sources, including plants and fungi, and have been studied for their potential biological activities. Some benzopyrans have been found to have anti-inflammatory, antioxidant, and anticancer properties. However, some benzopyrans can also be toxic or have other adverse health effects, so it is important to study their properties and potential uses carefully.

Electric stimulation, also known as electrical nerve stimulation or neuromuscular electrical stimulation, is a therapeutic treatment that uses low-voltage electrical currents to stimulate nerves and muscles. It is often used to help manage pain, promote healing, and improve muscle strength and mobility. The electrical impulses can be delivered through electrodes placed on the skin or directly implanted into the body.

In a medical context, electric stimulation may be used for various purposes such as:

1. Pain management: Electric stimulation can help to block pain signals from reaching the brain and promote the release of endorphins, which are natural painkillers produced by the body.
2. Muscle rehabilitation: Electric stimulation can help to strengthen muscles that have become weak due to injury, illness, or surgery. It can also help to prevent muscle atrophy and improve range of motion.
3. Wound healing: Electric stimulation can promote tissue growth and help to speed up the healing process in wounds, ulcers, and other types of injuries.
4. Urinary incontinence: Electric stimulation can be used to strengthen the muscles that control urination and reduce symptoms of urinary incontinence.
5. Migraine prevention: Electric stimulation can be used as a preventive treatment for migraines by applying electrical impulses to specific nerves in the head and neck.

It is important to note that electric stimulation should only be administered under the guidance of a qualified healthcare professional, as improper use can cause harm or discomfort.

An amino acid sequence is the specific order of amino acids in a protein or peptide molecule, formed by the linking of the amino group (-NH2) of one amino acid to the carboxyl group (-COOH) of another amino acid through a peptide bond. The sequence is determined by the genetic code and is unique to each type of protein or peptide. It plays a crucial role in determining the three-dimensional structure and function of proteins.

An oocyte, also known as an egg cell or female gamete, is a large specialized cell found in the ovary of female organisms. It contains half the number of chromosomes as a normal diploid cell, as it is the product of meiotic division. Oocytes are surrounded by follicle cells and are responsible for the production of female offspring upon fertilization with sperm. The term "oocyte" specifically refers to the immature egg cell before it reaches full maturity and is ready for fertilization, at which point it is referred to as an ovum or egg.

I must clarify that the term "Guinea Pigs" is not typically used in medical definitions. However, in colloquial or informal language, it may refer to people who are used as the first to try out a new medical treatment or drug. This is known as being a "test subject" or "in a clinical trial."

In the field of scientific research, particularly in studies involving animals, guinea pigs are small rodents that are often used as experimental subjects due to their size, cost-effectiveness, and ease of handling. They are not actually pigs from Guinea, despite their name's origins being unclear. However, they do not exactly fit the description of being used in human medical experiments.

Transient receptor potential vanilloid (TRPV) cation channels are a subfamily of transient receptor potential (TRP) channels, which are non-selective cation channels that play important roles in various physiological processes such as nociception, thermosensation, and mechanosensation. TRPV channels are activated by a variety of stimuli including temperature, chemical ligands, and mechanical forces.

TRPV channels are composed of six transmembrane domains with intracellular N- and C-termini. The TRPV subfamily includes six members: TRPV1 to TRPV6. Among them, TRPV1 is also known as the vanilloid receptor 1 (VR1) and is activated by capsaicin, the active component of hot chili peppers, as well as noxious heat. TRPV2 is activated by noxious heat and mechanical stimuli, while TRPV3 and TRPV4 are activated by warm temperatures and various chemical ligands. TRPV5 and TRPV6 are primarily involved in calcium transport and are activated by low pH and divalent cations.

TRPV channels play important roles in pain sensation, neurogenic inflammation, and temperature perception. Dysfunction of these channels has been implicated in various pathological conditions such as chronic pain, inflammatory diseases, and cancer. Therefore, TRPV channels are considered promising targets for the development of novel therapeutics for these conditions.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

Calcium carbonate is a chemical compound with the formula CaCO3. It is a common substance found in rocks and in the shells of many marine animals. As a mineral, it is known as calcite or aragonite.

In the medical field, calcium carbonate is often used as a dietary supplement to prevent or treat calcium deficiency. It is also commonly used as an antacid to neutralize stomach acid and relieve symptoms of heartburn, acid reflux, and indigestion.

Calcium carbonate works by reacting with hydrochloric acid in the stomach to form water, carbon dioxide, and calcium chloride. This reaction helps to raise the pH level in the stomach and neutralize excess acid.

It is important to note that excessive use of calcium carbonate can lead to hypercalcemia, a condition characterized by high levels of calcium in the blood, which can cause symptoms such as nausea, vomiting, constipation, confusion, and muscle weakness. Therefore, it is recommended to consult with a healthcare provider before starting any new supplement regimen.

"Xenopus laevis" is not a medical term itself, but it refers to a specific species of African clawed frog that is often used in scientific research, including biomedical and developmental studies. Therefore, its relevance to medicine comes from its role as a model organism in laboratories.

In a broader sense, Xenopus laevis has contributed significantly to various medical discoveries, such as the understanding of embryonic development, cell cycle regulation, and genetic research. For instance, the Nobel Prize in Physiology or Medicine was awarded in 1963 to John R. B. Gurdon and Sir Michael J. Bishop for their discoveries concerning the genetic mechanisms of organism development using Xenopus laevis as a model system.

Cyclic nucleotide-gated (CNG) channels are a type of ion channel found in the membranes of certain cells, particularly in the sensory neurons of the visual and olfactory systems. They are called cyclic nucleotide-gated because they can be activated or regulated by the binding of cyclic nucleotides, such as cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP), to the intracellular domain of the channel.

CNG channels are permeable to cations, including sodium (Na+) and calcium (Ca2+) ions, and their activation allows these ions to flow into the cell. This influx of cations can trigger a variety of cellular responses, such as the initiation of visual or olfactory signaling pathways.

CNG channels are composed of four subunits that form a functional channel. Each subunit has a cyclic nucleotide-binding domain (CNBD) in its intracellular region, which can bind to cyclic nucleotides and regulate the opening and closing of the channel. The CNBD is connected to the pore-forming region of the channel by a flexible linker, allowing for conformational changes in the CNBD to be transmitted to the pore and modulate ion conductance.

CNG channels play important roles in various physiological processes, including sensory perception, neurotransmission, and cellular signaling. Dysfunction of CNG channels has been implicated in several human diseases, such as retinitis pigmentosa, congenital stationary night blindness, and cystic fibrosis.

Calcium chloride is an inorganic compound with the chemical formula CaCl2. It is a white, odorless, and tasteless solid that is highly soluble in water. Calcium chloride is commonly used as a de-icing agent, a desiccant (drying agent), and a food additive to enhance texture and flavor.

In medical terms, calcium chloride can be used as a medication to treat hypocalcemia (low levels of calcium in the blood) or hyperkalemia (high levels of potassium in the blood). It is administered intravenously and works by increasing the concentration of calcium ions in the blood, which helps to regulate various physiological processes such as muscle contraction, nerve impulse transmission, and blood clotting.

However, it is important to note that calcium chloride can have adverse effects if not used properly or in excessive amounts. It can cause tissue irritation, cardiac arrhythmias, and other serious complications. Therefore, its use should be monitored carefully by healthcare professionals.

Potassium channels are membrane proteins that play a crucial role in regulating the electrical excitability of cells, including cardiac, neuronal, and muscle cells. These channels facilitate the selective passage of potassium ions (K+) across the cell membrane, maintaining the resting membrane potential and shaping action potentials. They are composed of four or six subunits that assemble to form a central pore through which potassium ions move down their electrochemical gradient. Potassium channels can be modulated by various factors such as voltage, ligands, mechanical stimuli, or temperature, allowing cells to fine-tune their electrical properties and respond to different physiological demands. Dysfunction of potassium channels has been implicated in several diseases, including cardiac arrhythmias, epilepsy, and neurodegenerative disorders.

Myocardial contraction refers to the rhythmic and forceful shortening of heart muscle cells (myocytes) in the myocardium, which is the muscular wall of the heart. This process is initiated by electrical signals generated by the sinoatrial node, causing a wave of depolarization that spreads throughout the heart.

During myocardial contraction, calcium ions flow into the myocytes, triggering the interaction between actin and myosin filaments, which are the contractile proteins in the muscle cells. This interaction causes the myofilaments to slide past each other, resulting in the shortening of the sarcomeres (the functional units of muscle contraction) and ultimately leading to the contraction of the heart muscle.

Myocardial contraction is essential for pumping blood throughout the body and maintaining adequate circulation to vital organs. Any impairment in myocardial contractility can lead to various cardiac disorders, such as heart failure, cardiomyopathy, and arrhythmias.

Nicardipine is a medication that belongs to a class of drugs called calcium channel blockers. It works by relaxing the muscles of your heart and blood vessels, which helps to lower your blood pressure and increase the supply of oxygen and blood to your heart.

Medically, Nicardipine is defined as a dihydropyridine calcium antagonist that is used in the management of hypertension and angina pectoris. It selectively inhibits the transmembrane influx of calcium ions into cardiac and vascular smooth muscle cells, which leads to vasodilation and decreased peripheral resistance. Nicardipine also reduces afterload and myocardial oxygen demand, making it useful in the treatment of hypertension and angina pectoris. It is available in immediate-release and extended-release formulations for oral administration, as well as in an intravenous formulation for use in hospital settings.

A smooth muscle within the vascular system refers to the involuntary, innervated muscle that is found in the walls of blood vessels. These muscles are responsible for controlling the diameter of the blood vessels, which in turn regulates blood flow and blood pressure. They are called "smooth" muscles because their individual muscle cells do not have the striations, or cross-striped patterns, that are observed in skeletal and cardiac muscle cells. Smooth muscle in the vascular system is controlled by the autonomic nervous system and by hormones, and can contract or relax slowly over a period of time.

The Ryanodine Receptor (RyR) is a calcium release channel located on the sarcoplasmic reticulum (SR), a type of endoplasmic reticulum found in muscle cells. It plays a crucial role in excitation-contraction coupling, which is the process by which electrical signals are converted into mechanical responses in muscle fibers.

In more detail, when an action potential reaches the muscle fiber's surface membrane, it triggers the opening of voltage-gated L-type calcium channels (Dihydropyridine Receptors or DHPRs) in the sarcolemma (the cell membrane of muscle fibers). This influx of calcium ions into the cytoplasm causes a conformational change in the RyR, leading to its own opening and the release of stored calcium from the SR into the cytoplasm. The increased cytoplasmic calcium concentration then initiates muscle contraction through interaction with contractile proteins like actin and myosin.

There are three isoforms of RyR: RyR1, RyR2, and RyR3. RyR1 is primarily found in skeletal muscle, while RyR2 is predominantly expressed in cardiac muscle. Both RyR1 and RyR2 are large homotetrameric proteins with a molecular weight of approximately 2.2 million Daltons. They contain multiple domains including an ion channel pore, regulatory domains, and a foot structure that interacts with DHPRs. RyR3 is more widely distributed, being found in various tissues such as the brain, smooth muscle, and some types of neurons.

Dysfunction of these channels has been implicated in several diseases including malignant hyperthermia, central core disease, catecholaminergic polymorphic ventricular tachycardia (CPVT), and certain forms of heart failure.

Ryanodine is not a medical condition or term, but it is a chemical compound that interacts with ryanodine receptors (RyRs), which are calcium release channels found in the sarcoplasmic reticulum of muscle cells. Ryanodine receptors play a crucial role in excitation-contraction coupling, which is the process by which electrical signals trigger muscle contractions.

Ryanodine itself is a plant alkaloid that was initially isolated from the South American shrub Ryania speciosa. It can bind to and inhibit ryanodine receptors, altering calcium signaling in muscle cells. This ability of ryanodine to modulate calcium release has made it a valuable tool in researching excitation-contraction coupling and related processes.

In some cases, the term "ryanodine" may be used in a medical context to refer to the effects of ryanodine or ryanodine receptor modulation on muscle function, particularly in relation to diseases associated with calcium handling abnormalities. However, it is not a medical condition per se.

Transient Receptor Potential Melastatin (TRPM) cation channels are a subfamily of the transient receptor potential (TRP) channel superfamily, which are non-selective cation channels that play important roles in various cellular processes such as sensory perception, cell proliferation, and migration.

The TRPM subfamily consists of eight members (TRPM1-8), each with distinct functional properties and expression patterns. These channels are permeable to both monovalent and divalent cations, including calcium (Ca^2+^) and magnesium (Mg^2+^).

TRPM channels can be activated by a variety of stimuli, such as changes in temperature, voltage, osmolarity, and chemical ligands. For example, TRPM8 is known to be activated by cold temperatures and menthol, while TRPV1 is activated by heat and capsaicin.

Dysregulation of TRPM channels has been implicated in various pathological conditions, including pain, neurodegenerative diseases, and cancer. Therefore, understanding the structure and function of these channels may provide insights into potential therapeutic targets for these conditions.

Spider venoms are complex mixtures of bioactive compounds produced by the specialized glands of spiders. These venoms are primarily used for prey immobilization and defense. They contain a variety of molecules such as neurotoxins, proteases, peptides, and other biologically active substances. Different spider species have unique venom compositions, which can cause different reactions when they bite or come into contact with humans or other animals. Some spider venoms can cause mild symptoms like pain and swelling, while others can lead to more severe reactions such as tissue necrosis or even death in extreme cases.

Muscle contraction is the physiological process in which muscle fibers shorten and generate force, leading to movement or stability of a body part. This process involves the sliding filament theory where thick and thin filaments within the sarcomeres (the functional units of muscles) slide past each other, facilitated by the interaction between myosin heads and actin filaments. The energy required for this action is provided by the hydrolysis of adenosine triphosphate (ATP). Muscle contractions can be voluntary or involuntary, and they play a crucial role in various bodily functions such as locomotion, circulation, respiration, and posture maintenance.

Acid-sensing ion channels (ASICs) are a type of ion channel protein found in nerve cells (neurons) that are activated by acidic environments. They are composed of homomeric or heteromeric combinations of six different subunits, designated ASIC1a, ASIC1b, ASIC2a, ASIC2b, ASIC3, and ASIC4. These channels play important roles in various physiological processes, including pH homeostasis, nociception (pain perception), and mechanosensation (the ability to sense mechanical stimuli).

ASICs are permeable to both sodium (Na+) and calcium (Ca2+) ions. When the extracellular pH decreases, the channels open, allowing Na+ and Ca2+ ions to flow into the neuron. This influx of cations can depolarize the neuronal membrane, leading to the generation of action potentials and neurotransmitter release.

In the context of pain perception, ASICs are activated by the acidic environment in damaged tissues or ischemic conditions, contributing to the sensation of pain. In addition, some ASIC subunits have been implicated in synaptic plasticity, learning, and memory processes. Dysregulation of ASIC function has been associated with various pathological conditions, including neuropathic pain, ischemia, epilepsy, and neurodegenerative diseases.

This is because adrenergic stimulation by agonists results in normal calcium channel regulation. If these adrenergic receptors ... Kerns, William (2007). "Management of β-Adrenergic Blocker and Calcium Channel Antagonist Toxicity". Emergency Medicine Clinics ... there will be an excess in calcium channel inhibition, which causes most of these problems. Adrenergic receptor Alpha blocker ... A receptor's agonist does not bind to its allosteric binding site. The binding of a non-competitive antagonist is irreversible ...
The most widely used tocolytics include beta agonists, calcium channel blockers, and magnesium sulfate. The goal of ...
Current evidence suggests that first line treatment with β2 agonists, calcium channel blockers, or NSAIDs to prolong pregnancy ... calcium channel blockers, oxytocin receptor antagonists and combinations of tocolytics. Calcium-channel blockers (such as ... Commonly used tocolytic medications include β2 agonists, calcium channel blockers, NSAIDs, and magnesium sulfate. These can ... Davis, W. B.; Wells, S. R.; Kuller, J. A.; Thorp, J. M. (March 1997). "Analysis of the risks associated with calcium channel ...
Bhugra P, Gulati OD (1996). "Interaction of calcium channel blockers with different agonists in aorta from normal and diseased ... Bhugra P, Gulati OD (2001). "Influence of chronic treatment of rats with isoprenaline and calcium channel blockers on response ...
β1 agonists stimulate adenylyl cyclase activity and opening of calcium channel (cardiac stimulants; used to treat cardiogenic ... Prenalterol Xamoterol β2 agonists stimulate adenylyl cyclase activity and closing of calcium channel (smooth muscle relaxants; ... Beta adrenergic agonists or beta agonists are medications that relax muscles of the airways, causing widening of the airways ... In general, pure beta-adrenergic agonists have the opposite function of beta blockers: beta-adrenoreceptor agonist ligands ...
... is a chemical compound that functions as an L-type calcium channel agonist. Bay K8644 is used primarily as a ... Bay K8644 targets L-type voltage-gated calcium channels. It is the first positive inotropic agent shown to act specifically and ... Calcium channel openers, Nitro compounds, All stub articles, Cardiovascular system drug stubs). ... directly on calcium channels. (±)-Bay K8644 at Sigma-Aldrich CID 2303 from PubChem Thomas, G; Chung, M; Cohen, CJ (January 1985 ...
1988). "Some Chemical Properties of Maitotoxin, a Putative Calcium Channel Agonist Isolated from a Marine Dinoflagellate". J. ... Non-protein ion channel toxins, Calcium channel openers, Conjugated dienes, Sulfate esters, Heterocyclic compounds with 7 or ... Maitotoxin activates extracellular calcium channels, leading to an increase in levels of cytosolic Ca2+ ions. The exact ... and turns it into an ion channel, similar to how palytoxin turns the Na+/K+-ATPase into an ion channel. Ultimately, a ...
In addition, β2 agonists open large conductance calcium-activated potassium channels and thereby tend to hyperpolarize airway ... Discovery and development of β2 agonists β3-adrenergic agonist Eric, Hsu; Tushar, Bajaj (2022). "Beta 2 Agonists". NCBI. PMID ... Beta2-adrenergic agonists, also known as adrenergic β2 receptor agonists, are a class of drugs that act on the β2 adrenergic ... Like other β adrenergic agonists, they cause smooth muscle relaxation. β2 adrenergic agonists' effects on smooth muscle cause ...
Monoterpenoids also induce agonist-specific desensitization of TRPV3 channels in a calcium-independent manner. Resolvin E1 ( ... 2009). "Monoterpenoids Induce Agonist-Specific Desensitization of Transient Receptor Potential Vanilloid-3 (TRPV3) ion Channels ... Farnesyl pyrophosphate is an endogenous agonist of TRPV3, while incensole acetate from frankincense also acts as an agonist at ... The protective effects of the natural product, incensole acetate were partially mediated by TRPV3 channels. The TRPV3 channel ...
In the visual system, cannabinoids agonist induce a dose dependent modulation of calcium, chloride and potassium channels. This ... Negatively to D-type outward potassium channels Negatively to N-type and P/Q-type calcium channels. The CB1 receptor is encoded ... including the positively influenced inwardly rectifying potassium channels (=Kir or IRK), and calcium channels, which are ... The inverse agonist MK-9470 makes it possible to produce in vivo images of the distribution of CB1 receptors in the human brain ...
Different modes of calcium channel gating behavior favored by dihydropyridine agonists and antagonists. Nature 311:538-544. ( ... Calcium channel selectivity for divalent and monovalent cations. Voltage and concentration dependence of single channel current ... Lansman is known for his fundamental research on calcium channels in nerve and muscle and their role in normal physiology and ... He subsequently identified ion channels that transduce mechanical forces into the entry of calcium into blood vessels and in ...
... calcium-channel blockers and beta-adrenergic agonists, may increase the risk. Anesthesia: General anesthetics during surgery ... "Urologic Emergencies". Urology Channel Portal. 10 February 2010. Archived from the original on 10 March 2010. Özveren B, Keskin ... Medications: Anticholinergics and medications with anticholinergic properties, alpha-adrenergic agonists, opiates, nonsteroidal ...
... calcium channel blockers, PPAR-γ agonists, curcuminoids, ethanol, NMDA antagonists, caffeine. In addition to traditional ... Langham J, Goldfrad C, Teasdale G, Shaw D, Rowan K (2003). "Calcium channel blockers for acute traumatic brain injury". The ... Yi JH, Park SW, Brooks N, Lang BT, Vemuganti R (December 2008). "PPARgamma agonist rosiglitazone is neuroprotective after ... Forsyth RJ, Jayamoni B, Paine TC (October 2006). "Monoaminergic agonists for acute traumatic brain injury". The Cochrane ...
... calcium channel agonists MeSH D27.505.519.562.249 - calcium channel blockers MeSH D27.505.519.562.374 - ionophores MeSH D27.505 ... calcium channel agonists MeSH D27.505.954.411.793.610 - nasal decongestants MeSH D27.505.954.411.918 - vasodilator agents MeSH ... calcium channel blockers MeSH D27.505.954.411.207 - cardioplegic solutions MeSH D27.505.954.411.222 - cardiotonic agents MeSH ... 500 - potassium channel blockers MeSH D27.505.519.562.750 - sodium channel blockers MeSH D27.505.519.562.812 - sodium chloride ...
Alpha/Beta Adrenergic Agonists, Calcium Channel Blockers, Anticoagulants, Cardiovascular, Opioid Analgesics". emedicine. ... "Dopamine agonists and the risk of cardiac-valve regurgitation". N. Engl. J. Med. 356 (1): 29-38. doi:10.1056/NEJMoa062222. PMID ... calcium blockers and avoiding very strenuous activity. As of 2007, the American Heart Association no longer recommends ... "Valvular heart disease and the use of dopamine agonists for Parkinson's disease". N. Engl. J. Med. 356 (1): 39-46. doi:10.1056/ ...
Mu-opioid receptor agonists, Serotonin-norepinephrine reuptake inhibitors, Sigma agonists, Calcium channel blockers, All stub ...
... dopamine agonists, TNF inhibitors, calcium channel blockers (especially verapamil and diltiazem), salbutamol, and tamsulosin. ... Certain calcium channel blockers, such as diltiazem and verapamil, are known to decrease the force with which the heart ejects ... Tetrandrine can lead to low blood pressure through inhibition of L-type calcium channels. Yohimbine can exacerbate heart ... alpha-2 adrenergic receptor agonists, minoxidil, itraconazole, cilostazol, anagrelide, stimulants (e.g., methylphenidate), ...
... a central α2-agonist), diltiazem (a calcium channel blocker), and prazosin (an α1-blocker) on pulse pressure and found that, ...
... calcium channel blockers, diuretics, sedatives, alpha-adrenergic agonist, alpha 1 antagonists). Urinary symptoms may include ... For urinary retention, cholinergics (muscarinic agonists) like bethanechol can improve the squeezing ability of the bladder. ...
... is a chemical compound which acts as an "agonist" (i.e. channel opener) of the TRPML family of calcium channels. It has ... February 2018). "Robust lysosomal calcium signaling through channel TRPML1 is impaired by lysosomal lipid accumulation". FASEB ... Feng X, Xiong J, Lu Y, Xia X, Zhu MX (December 2014). "Differential mechanisms of action of the mucolipin synthetic agonist, ML ... on insect TRPML and mammalian TRPML1". Cell Calcium. 56 (6): 446-56. doi:10.1016/j.ceca.2014.09.004. PMC 4252876. PMID 25266962 ...
... and calcium channel blockers). Inverse agonists have opposite actions to those of agonists but the effects of both of these can ... Both endogenous and exogenous inverse agonists have been identified, as have drugs at ligand gated ion channels and at G ... An agonist increases the activity of a receptor above its basal level, whereas an inverse agonist decreases the activity below ... Agonists for GABAA receptors (such as muscimol) create a relaxant effect, whereas inverse agonists have agitation effects (for ...
... and other β2 receptor agonists also increase the conductance of channels sensitive to calcium and potassium ions, ... While preferred over agents such as atosiban and ritodrine, its role has largely been replaced by the calcium channel blocker ... It is a short-acting β2 adrenergic receptor agonist which works by causing relaxation of airway smooth muscle. It is used to ... The 1972 Munich Olympics were the first Olympics where anti-doping measures were deployed, and at that time β2 agonists were ...
Also, roscovitine can either act as an agonist or antagonist for the P-type calcium channels in the presynaptic membrane. ... The P-type calcium channel is a type of voltage-dependent calcium channel. Similar to many other high-voltage-gated calcium ... type calcium channels are voltage-dependent calcium channels that are classified under the high voltage activated class channel ... P-type calcium channel blockers act to impede the flow of calcium. The blocking of calcium currents may cause the organism to ...
Calcium channel blockers, Chloroarenes, GABA analogues, GABAB receptor agonists, Gamma-Amino acids, Prodrugs, All stub articles ...
... to L-type voltage-sensitive Ca2+ calcium channel. Taniyama, Yusuke; Suzuki, Takashi; Mikami, Yoshiki; Moriya, Takuya; Satomi, ... Agonists of the somatostatin receptor had been long established as an imaging agent, with the first agonist Ga-DOTATOC coming ... Gallium-containing agonists had already been established as an imaging agent. Lutetium-containing agonists were used as a ... The structure of somatostatin receptor antagonists are similar to that of the agonists. Some agonists were already approved by ...
... to L-type voltage-sensitive Ca2+ calcium channel. Taniyama, Yusuke; Suzuki, Takashi; Mikami, Yoshiki; Moriya, Takuya; Satomi, ... Agonists of the somatostatin receptor had been long established as an imaging agent, with the first agonist Ga-DOTATOC coming ... Gallium-containing agonists had already been established as an imaging agent. Lutetium-containing agonists were used as a ... The structure of somatostatin receptor antagonists is similar to that of the agonists. Some agonists were already approved by ...
... which is responsible for turning on calcium inflow channels. A decrease in activation of calcium channels will therefore result ... β2-adrenergic receptor agonists, and clonidine. Some evidence suggests that sotalol should be avoided in the setting of heart ... As with other beta blockers, it may interact with calcium channel blockers, catecholamine-depleting drugs, insulin or ... In consideration of these important properties of calcium, two conclusions can be drawn. First, with less calcium in the cell, ...
... and a neuronal calcium channel blocker. Capsaicin is able to excite and desensitize C-fibers. As such, it is not only able to ... It has a melting point of 71.5-74.5 °C. Zucapsaicin mediates an antinociceptive action via acting as an agonist at TRPV1. TRPV1 ... activation of calcium-dependent protein kinase C isoforms and subsequent channel phosphorylation. Desensitization involves both ... It is a modulator of transient receptor potential cation channel subfamily V member 1 (TRPV-1), also known as the vanilloid or ...
... calcium channels. Depolarization may be brought about by stretching of the cell, agonist-binding its G protein-coupled receptor ... opening of the L-type calcium channel permits influx of calcium into the cell. The calcium binds to the calcium release ... High-voltage-gated calcium channels include the neural N-type channel blocked by ω-conotoxin GVIA, the R-type channel (R stands ... Voltage-gated calcium channels (VGCCs), also known as voltage-dependent calcium channels (VDCCs), are a group of voltage-gated ...
Calcium can also act as a co-agonist at the IP3 receptor. A selective agonist is selective for a specific type of receptor. E.g ... Colquhoun D (January 2006). "Agonist-activated ion channels". British Journal of Pharmacology. 147 (S1): S17-S26. doi:10.1038/ ... Inverse agonists exert the opposite pharmacological effect of a receptor agonist, not merely an absence of the agonist effect ... It might be argued that the endogenous agonist is simply a partial agonist in that tissue. An irreversible agonist is a type of ...
Effects of the calcium channel agonist, BAY K 8644, on electrical activity in mouse pancreatic B-cells.. ... Effects of the calcium channel agonist, BAY K 8644, on electrical activity in mouse pancreatic B-cells. ...
Calcium channel blockers. Class Summary. Calcium channel blockers inhibit the movement of calcium ions across the cell membrane ... Adrenergic Agonists. Class Summary. These agents act directly on alpha- and beta-receptors, producing effects similar to those ... During depolarization, diltiazem inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular ... Dobutamine is a synthetic direct-acting catecholamine and beta-receptor agonist. It increases cardiac contractility and output ...
This is because adrenergic stimulation by agonists results in normal calcium channel regulation. If these adrenergic receptors ... Kerns, William (2007). "Management of β-Adrenergic Blocker and Calcium Channel Antagonist Toxicity". Emergency Medicine Clinics ... there will be an excess in calcium channel inhibition, which causes most of these problems. Adrenergic receptor Alpha blocker ... A receptors agonist does not bind to its allosteric binding site. The binding of a non-competitive antagonist is irreversible ...
Drugs such as adrenoceptor agonists, muscarinic agonists, nitrates, and calcium ... of the drugs that stimulate or inhibit smooth muscle contraction do so by regulating the concentration of intracellular calcium ... Drugs such as adrenoceptor agonists, muscarinic agonists, nitrates, and calcium channel blockers all affect smooth muscle. ... For example, salbutamol was discovered as a specific β2-adrenoceptor agonist. It is used to treat asthma and is a great ...
It is thought that endothelins act as endogenous agonists of dihydropyridine-sensitive calcium channels. The most striking ... A. Calcium Supplementation. Several authors have reported reduced urinary excretion of calcium during preeclampsia and for ... In this study there was no decrease in the incidence or severity of preeclampsia in the group receiving calcium. However, ... In addition, abnormal intracellular calcium metabolism in platelets and red blood cells has been demonstrated in women with ...
Beta blockers, calcium-channel blockers, and alpha2-agonists are associated with this toxidrome.. The primary symptoms of the ... For example, glucagon and calcium can be given for beta-blocker and calcium-channel blocker overdoses, respectively. IV fluids ...
Calcium Channel Blockers. Class Summary. Migraine prophylaxis has been reported with various calcium channel blockers, ... The calcium channel blocker with the highest evidence of efficacy is flunarizine, which is not available in the United States. ... These medications are migraine preventatives; they include flunarizine, a calcium channel blocker; gabapentin; riboflavin; and ... Therapeutic activity of the serotonin 5-HT1 receptor agonists (ie, triptans) in migraine is most likely attributed to agonist ...
Intracellular calcium strongly potentiates agonist-activated TRPC5 channels. References Authors * Blair NT Show Other ...
... and in combination with a newly developed calcium channel gating modifier (the novel calcium channel agonist GV-58). These ... MCell is also being used to evaluate the effects of the current treatment for LEMS that target calcium channel activation ... each consisting of a synaptic vesicle and associated voltage gated calcium channels (VGCCs). Lambert-Eaton myasthenic syndrome ... during an action potential (the potassium channel blocker DAP) alone, ...
... has shown selectivity toward P-type calcium channel and enhanced the agonist-induced tail flick antinociception when co- ... Animal venoms or purified toxins evoke complex effects on ion channels, mainly sodium, potassium and calcium channels (56, 66, ... Huwentoxin-I, a N-type calcium channel blocker isolated from the venom of the Chinese tarantula Ornithoctonus huwena, has ... A toxin from the spider Phoneutria nigriventer that blocks calcium channels coupled to exocytosis. Br J Pharmacol. 1997;122(3): ...
Learn and reinforce your understanding of Opioid agonists, mixed agonist-antagonists and partial agonists. ... mixed agonist-antagonists and partial agonists Videos, Flashcards, High Yield Notes, & Practice Questions. ... Calcium channels. opioid effect on p. 572. Diarrhea. opioids for p. 572 ... Examples of opioid agonists include morphine, codeine, and oxycodone. Mixed agonist-antagonists bind to and activate opioid ...
Calcium channel blockers in the management of low-tension and open-angle glaucoma. Am J Ophthalmol. 1993 May 15. 115(5):608-13 ... Prostaglandin agonists. Class Summary. For reduction of IOP in patients intolerant to other IOP-lowering medications or who do ... Alpha2-adrenergic agonists. Class Summary. Decrease IOP pressure by reducing aqueous humor production. ... Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Used to treat open-angle ...
The study reported that the extract might block either calcium channels, sodium channels, or NMDA receptors, or has GABA ... agonist activity.. Anticancer. The main pathway for the anticancer activity of Moringa species is by inhibiting proliferation ... Other than having a high concentration of vitamin A, vitamin C, potassium, and calcium, the plant contains all the essential ... 2016a) suggested that the extract blocked Ca2+ channels during this activity. The endothelium might have stimulated relaxing ...
... the T149A 5-HT1A receptor mutant failed to block the influx of calcium induced by calcium channel agonist (±)-Bay K8644, ... and to inhibition of calcium channel activation (mediated by βγ subunits of Go) but plays a minor role in coupling to αi- ... A 2.6-fold increase in intracellular calcium (due to phospholipase C-mediated calcium mobilization) was observed for the wild- ... In both cell lines, the T149A mutant displayed similar agonist affinities as the wild-type receptor. In Ltk− cells, the T149A 5 ...
1996, Calcium-dependent modulation of the agonist affinity of the mammalian olfactory cyclic nucleotide-gated channel by ... Liquid Junction Potentials, Ion Channels, Structure & Function of Ion Channels, Ligand gated ion channels, Unstirred Layer ... Barry PH; Qu W; Moorhouse AJ, 2008, Biophysics of CNG Ion Channels, in Martinac B (ed.), Sensing with Ion Channels, edn. ... Hallani M; Lynch JW; Barry PH, 1998, Characterisation of calcium-activated chloride channels in patches excised from the ...
We next tested the hypothesis that mGluR agonists inhibited kainate-evoked calcium rises by blocking a calcium channel. Kainate ... Most of the potassium-evoked calcium rise was blocked by nimodipine; other calcium channel antagonists were not tested. Calcium ... Increases in glial calcium could result in the opening of calcium-activated potassium channels (Quandt and MacVicar, 1986; ... Part of the calcium rise with kainate stimulation may be attributable to activation of voltage-gated calcium channels. ...
Aged; Apoptosis; Cadherins; Calcium Channel Agonists; Cell Differentiation; Cells, Cultured; Collagen; Extracellular Matrix; ... In order to establish this, we disrupted calcium signalling by blocking stretch-activated calcium channel (SACC) in human MSCs ... potential of human bone marrow stromal cells by uniaxial stretching affected by stretch-activated calcium channel agonist ... potential of human bone marrow stromal cells by uniaxial stretching affected by stretch-activated calcium channel agonist ...
Application to calcium channel agonists Analusis 28, 637-642 (2000). Computational QSAR model combined molecular descriptors ...
药动学] Calcium Channel Agonists [英文释义] The physiologically active form of vitamin D. It is formed pri. ...
... central alpha-2 agonists, beta-blockers, and alpha-blockers), calcium channel blockers, angiotensin-converting enzyme ... Chapter 7 Connexin-Based Channels and RhoA/ROCK Pathway in A... By Gonzalo I. Gómez, Victoria Velarde and Juan C. Sáe... ...
Asthma remedies - Beta-agonists, hypotension medications - beta blockers, calcium channel blockers. Centrally acting agents ( ...
Baum VC: Will the calcium channel agonist BAY K 8644 inhibit halothane-induced impairment of calcium current? Anesth Analg 1992 ... McDonald TF, Pelzer S, Trautwein W, Pelzer DJ: Regulation and modulation of calcium channels in cardiac, skeletal, and smooth ... Allen TJ: Temperature dependence of macroscopic L-type calcium channel currents in single guinea pig ventricular myocytes. J ... Temperature-independent Inhibition of L-Type Calcium Currents by Halothane and Sevoflurane in Human Atrial Cardiomyocytes Rocco ...
Calcium channel agonists, antagonists and modulators * AM ester guide Find the best indicator and ionophore for imaging Ca2+ ... Agonists, activators, antagonists and inhibitors. Cell lines and Lysates. Multiplex Assays. By research area. Cancer. ... Calcium (Ca2+) is an important ubiquitous second messenger, involved in the regulation of a diverse range of cellular processes ... Fluo-5 AM is an analogue of Fluo-4 with reduced calcium binding affinity, for this reason it is suitable for detecting ...
Kappa-opioid CPI-203 receptor agonists have also been shown to inhibit calcium channels. Calcium channel inhibitors have ... This might clarify that in some studies kappa-opioid receptor agonists attenuate nicotine and opioid withdrawal symptomatology ...
DG01575 Calcium channel blocker. DG01496 Calcium channel L type blocker. DG01456 Adrenergic receptor agonist. DG01653 ... Ion channels. Voltage-gated ion channels. Calcium channels. CACNA1-L. D03914 Dronedarone hydrochloride (USP) ,US,. Potassium ... DG01575 Calcium channel blocker. DG01496 Calcium channel L type blocker. DG00207 Dronedarone. DG01456 Adrenergic receptor ... DG01575 Calcium channel blocker. DG01496 Calcium channel L type blocker. DG00207 Dronedarone. D03914 Dronedarone hydrochloride ...
Central agonists, Calcium channel blockers ,vasodilators, Ace inhibitors, Blood pressure should always remain in the normal ... low calcium intake. What is Treatment of Hypertension? November 21, 2022 Hypertension November 11, 2022 Eitiology of ...
Neurosteroids Shift Partial Agonist Activation of GABAA Receptor Channels from Low- to High-Efficacy Gating Patterns. Matt T. ... Yue DT, Herzig S, Marban E ( 1990) Beta-adrenergic stimulation of calcium channels occurs by potentiation of high-activity ... Neurosteroids Shift Partial Agonist Activation of GABAA Receptor Channels from Low- to High-Efficacy Gating Patterns ... Neurosteroids Shift Partial Agonist Activation of GABAA Receptor Channels from Low- to High-Efficacy Gating Patterns ...
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Vitamin B6: (or as in a B Complex) works as a diuretic, a calcium channel blocker, a central alpha agonist, and an angiotensin ... Taurine: works as a diuretic, a calcium channel blocker, a central alpha agonist, an angiotensin receptor blocker ... Celery (powder): works as a diuretic, calcium channel blocker, central alpha agonist, an angiotensin receptor blocker ... and other elements that act as calcium channel blockers, central alpha agonists, angiotensin receptor blockers, angiotensin- ...
  • Drugs such as adrenoceptor agonists, muscarinic agonists, nitrates, and calcium channel blockers all affect smooth muscle. (britannica.com)
  • thus, diag- -agonists, calcium channel blockers, mal heart rate response in some nosis relies heavily on results of labo- or xanthine derivatives. (cdc.gov)
  • Beta blockers, calcium-channel blockers, and alpha2-agonists are associated with this toxidrome. (logicalimages.com)
  • Allosteric conversion of partial to full agonism may be a general mechanism for reversibly scaling the efficacy of GABA A receptors to endogenous partial agonists. (jneurosci.org)
  • Although the physiological relevance of endogenous partial agonists remains poorly understood, the possibility of reversible augmentation of partial agonist efficacy by endogenous modulators raises the interesting possibility of plasticity at the level of agonist-dependent gating. (jneurosci.org)
  • Opioid full agonists are drugs that bind to and activate opioid receptors in the body . (osmosis.org)
  • Mixed agonist-antagonists bind to and activate opioid receptors to a certain extent, but also have the ability to block or inhibit the effects of other opioids . (osmosis.org)
  • Although GABA activates synaptic (αβγ) GABA A receptors with high efficacy, partial agonist activation of αβγ isoforms and GABA activation of the primary extrasynaptic (αβδ) GABA A receptors are limited to low-efficacy activity, characterized by minimal desensitization and brief openings. (jneurosci.org)
  • It is even more intriguing to consider the potential plasticity of allosteric modulation given the observation of agonist-dependent functional properties of GABA A receptors. (jneurosci.org)
  • Saw palmetto extract (SPE), used widely for the treatment of benign prostatic hyperplasia (BPH) has been shown to bind alpha(1)-adrenergic, muscarinic and 1,4-dihydropyridine (1,4-DHP) calcium channel antagonist receptors. (nih.gov)
  • The results suggest that lauric acid and oleic acid bind noncompetitively to alpha(1)-adrenergic, muscarinic and 1,4-DHP calcium channel antagonist receptors. (nih.gov)
  • The maximum effect of the drug may be produced even if not all receptors are bound in the presence of which of the following: A. Full agonist B. Partial agonist C. Spare receptors D. Inert binding site E. Effector 7. (kupdf.net)
  • Thus far, the pharmacological treatment of asthma and COPD mainly relies upon β2 agonists and muscarinic antagonists, which can affect β2-adrenergic and muscarinic receptors, respectively. (biomedcentral.com)
  • Through the regulation of signal pathways related to G protein-coupled receptors, the reduction of intracellular calcium, and the subsequent opening of VDCC/NSCC, airway smooth muscle tone could be relaxed [ 6 , 7 ]. (biomedcentral.com)
  • Kappa-opioid CPI-203 receptor agonists have also been shown to inhibit calcium channels. (biopaqc.com)
  • This might clarify that in some studies kappa-opioid receptor agonists attenuate nicotine and opioid withdrawal symptomatology. (biopaqc.com)
  • This includes the receptor agonists, GATA transcription factors, sodium and calcium ion channels, and glutamine receptor antagonists. (theuniversalplant.com)
  • However, numerous studies have indicated that currently available bronchodilators, especially β2-agonists and muscarinic antagonists, have additive effects on safety, desensitization and tolerability [ 8 - 10 ]. (biomedcentral.com)
  • Most of the drugs that stimulate or inhibit smooth muscle contraction do so by regulating the concentration of intracellular calcium , which is involved in initiating the process of contraction. (britannica.com)
  • Intracellular calcium strongly potentiates agonist-activated TRPC5 channels. (yale.edu)
  • Changes in intracellular calcium not only modify glial physiology, but they also seem to be involved in complex intercellular communication networks (for review, see Finkbeiner, 1993 ). (jneurosci.org)
  • Fluo-5 AM is an analogue of Fluo-4 with reduced calcium binding affinity, for this reason it is suitable for detecting intracellular calcium levels that would saturate the Fluo-4 AM indicator. (abcam.com)
  • Antagonists reduce or block the signals of agonists. (wikipedia.org)
  • While competitive antagonists bind to the agonist or ligand binding site of the receptor reversibly, non-competitive antagonists can either bind to the ligand site or other site called the allosteric site. (wikipedia.org)
  • The self-biting provoked by (±)Bay K 8644 can be inhibited by pretreating the mice with dihydropyridine L type calcium channel antagonists such as nifedipine, nimodipine, or nitrendipine. (epiphanyasd.com)
  • An alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. (pharmfair.com)
  • Remodeling of the cardiac pacemaker L-type calcium current and its beta-adrenergic responsiveness in hypertension after neuronal NO synthase gene transfer. (ox.ac.uk)
  • We tested the hypothesis that beta-adrenergic hyperresponsiveness in the sinoatrial node (SAN) of the spontaneously hypertensive rat occurs at the level of the L-type calcium current because of altered cyclic nucleotide-dependent signaling. (ox.ac.uk)
  • Decreased calcium current after cardiac nNOS gene transfer contributes to the normalization of beta-adrenergic hyperresponsiveness in the SAN from hypertensive rats by modulating cyclic nucleotide signaling. (ox.ac.uk)
  • Thus, the Thr149 residue is directly involved in G protein coupling to calcium mobilization (mediated by βγ subunits of G i2 ) and to inhibition of calcium channel activation (mediated by βγ subunits of G o ) but plays a minor role in coupling to α i -mediated inhibition of cAMP accumulation. (aspetjournals.org)
  • The inhibition could be mimicked by the L-type calcium channel blocker nimodipine (1 μ m ) as well as by protein kinase C (PKC) activators phorbol 12,13-dibutyrate (10 μ m ) and phorbol 12-myristate 13-acetate (500 n m ), and blocked by the PKC inactivator (±)-1-(5-isoquinolinesulfonyl)-2-methylpiperazine (200 μ m ), suggesting a mechanism involving PKC modulation of L-type calcium channels. (jneurosci.org)
  • In hypothalamic neurons, modulators such as neuropeptide Y (NPY) and adenosine depress glutamatergic transmission by either a pertussis toxin (PTx)-sensitive G-protein-coupled pathway or by inhibition of voltage-activated calcium channels (VACCs). (jneurosci.org)
  • Besides, MC4R G233S mutant demonstrated an altered agonist-dependent inhibition of voltage-gated calcium channels type 2.2. (bvsalud.org)
  • Further research indicates that AELL mediate relaxation through voltage-dependent Ca 2+ channels (VDCC) and non-selective cation channels (NSCC) inhibition. (biomedcentral.com)
  • For example, glucagon and calcium can be given for beta-blocker and calcium-channel blocker overdoses, respectively. (logicalimages.com)
  • MCell is also being used to evaluate the effects of the current treatment for LEMS that target calcium channel activation during an action potential (the potassium channel blocker DAP) alone, and in combination with a newly developed calcium channel gating modifier (the novel calcium channel agonist GV-58). (psc.edu)
  • T oday's post was prompted by a reader who saw a very positive response from the L-type calcium channel blocker, Amlodipine. (epiphanyasd.com)
  • MK-801 is a non-competitive NMDA-channel blocker and glutamate antagonist that protects the brain of rats from ischaemic damage. (patentpc.com)
  • Opioid agonists are medications used mainly to control acute or chronic pain in particular situations. (osmosis.org)
  • Examples of opioid agonists include morphine , codeine , and oxycodone . (osmosis.org)
  • Calcium channel inhibitors have antidepressant-like effects and inhibit the release of norepinephrine. (biopaqc.com)
  • They work by blocking potassium-selective channels in the nerve membrane, thereby prolonging the electrical impulse in the nerve terminal and increasing the amount of acetylcholine released. (britannica.com)
  • Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. (medscape.com)
  • It has become less extensively used with the advent of more selective agonists. (pharmfair.com)
  • Furthermore, AELL-induced smooth muscle relaxation was partially mediated by blocking voltage-dependent Ca 2+ channels (VDCC) and non-selective cation channels (NSCC). (biomedcentral.com)
  • [5] Additionally, aortic insufficiency has been linked to the use of some medications, specifically medications containing fenfluramine or dexfenfluramine isomers and dopamine agonists . (iiab.me)
  • Cevimeline is in a class of medications called cholinergic agonists. (medlineplus.gov)
  • The current drugs used to block calcium channels were mainly developed to treat heart conditions. (epiphanyasd.com)
  • It is the most potent of the opiate agonists and is useful for the acute management of headache due to migraine. (medscape.com)
  • DI-fusion Effects of the calcium channel agonist, BAY K 8644, on. (ac.be)
  • Effects of the calcium channel agonist, BAY K 8644, on electrical activity in mouse pancreatic B-cells. (ac.be)
  • The L type calcium channel agonist (±)Bay K 8644 has been reported to cause characteristic motor abnormalities in adult mice. (epiphanyasd.com)
  • The neuromuscular junction is a reliable synapse in which reliability derives from the summed activity of numerous unreliable elements, each consisting of a synaptic vesicle and associated voltage gated calcium channels (VGCCs). (psc.edu)
  • We studied modulation of glutamate-evoked calcium rises in primary astrocyte cultures using fura-2 ratiometric digital calcium imaging. (jneurosci.org)
  • Suprachiasmatic nucleus (SCN) and cortical astrocytes showed striking differences in sensitivity to glutamate and to mGluR agonists, even after several weeks in culture. (jneurosci.org)
  • Verapamil blocks L type channels and T type channels, plus some potassium ion channels. (epiphanyasd.com)
  • This type of binding is reversible as increasing the concentration of agonist will outcompete the concentration of antagonist, resulting in receptor activation. (wikipedia.org)
  • A receptor's agonist does not bind to its allosteric binding site. (wikipedia.org)
  • If the non-competitive antagonist binds to the allosteric site and an agonist binds to the ligand site, the receptor will remain unactivated. (wikipedia.org)
  • In contrast, mGluRs modulated serotonin (5HT)-evoked calcium rises through a different mechanism. (jneurosci.org)
  • The type III mGluR agonist l -2-amino-4-phosphonobutyrate consistently inhibited 5HT-evoked calcium rises, whereas in a smaller number of cells quisqualate and L-CCG-I showed both inhibitory and additive effects. (jneurosci.org)
  • 10 This temperature-dependent behavior of calcium currents has also been observed in several other tissues, e.g. , in neurons or pancreatic β cells. (asahq.org)
  • In this study, we investigated the effects of TF extract on skin inflammation in an AD animal model and also investigated the mechanism responsible for the effects of TF extract in AD on the modulation of calcium channels and the activation of mast cells. (hindawi.com)
  • We investigated the pathogenicity of mutations in HEK293T cells expressing wild-type or mutant MC4R and found that both mutants exhibited reduced plasma membrane expression and altered agonist-induced cAMP responses, with no changes in basal activity. (bvsalud.org)
  • Blocking P channels might have protected Purkinje cells from death. (epiphanyasd.com)
  • In addition, L-type calcium current was measured in cells isolated from the SAN of transfected animals. (ox.ac.uk)
  • Unlike the mGluR-kainate interaction, which required a pretreatment with an mGluR agonist and was insensitive to pertussis toxin (PTx), the mGluR modulation of 5HT actions was rapid and was blocked by PTx. (jneurosci.org)
  • The unusual sensitivity of αβδ receptor channels to neurosteroid modulation prompted investigation of whether this high sensitivity was dependent on the δ subunit or the low-efficacy channel function that it confers. (jneurosci.org)
  • The present study demonstrates that the topical application of TF extract improves skin inflammation in AD mice, and the mechanism for this effect appears to be related to the modulation of calcium channels and mast cell activation. (hindawi.com)
  • We developed a model that assumes channel modulation is a pseudo-first-order process kinetically limited by free Ca 2+ . (silverchair.com)
  • Extracellular purine nucleotides appear capable of regulating plant development, defense and stress responses by acting in part as agonists of plasma membrane calcium channels. (edu.au)
  • Release of ADP from root epidermis would trigger ionotropic receptor-like activity in the plasma membrane, resulting in transient elevation of cytosolic free calcium. (edu.au)
  • Cardiac L-type calcium currents (ICa,L) are affected by volatile anesthetics, possibly contributing to their side effects. (asahq.org)
  • ANESTHETIC gases may interfere with cardiac ion channels. (asahq.org)
  • Ethaverine, a derivative of papaverine, inhibits cardiac L-type calcium channels. (aspetjournals.org)
  • We tested its effects on single, dihydropyridine-sensitive, L-type calcium channels from porcine cardiac muscle, incorporated into planar lipid bilayers. (aspetjournals.org)
  • To test whether the effect of ethaverine on open probability was due to a displacement of the dihydropyridine agonist, we studied the effect of ethaverine on the binding of [3H]nitrendipine to cardiac sarcolemma and found that ethaverine inhibited [3H]nitrendipine binding with a Ki of approximately 8.5 microM. (aspetjournals.org)
  • Because ethaverine is structurally related to verapamil, it is likely that ethaverine acts by binding to the verapamil binding sites on the L-type calcium channels to inhibit channel activation and dihydropyridine binding. (aspetjournals.org)
  • These mechanisms include the ability of lead to inhibit or mimic the action of calcium and to interact with proteins. (cdc.gov)
  • Acetylcholine binding causes ion channels to open and allows a local influx of positively charged ions into the muscle fibre, ultimately causing the muscle to contract. (britannica.com)
  • Although previous studies have reported that calcium signalling is involved in regulating many cellular processes in many cell types, its role in managing cellular responses to tensile loading (mechanotransduction) of MSCs has not been fully elucidated. (um.edu.my)
  • This confirms that ADP could elicit calcium-based responses distinct to those of ATP, which have been shown previously to involve production of extracellular reactive oxygen species. (edu.au)
  • His interests and those of his research groups have included exploring the mechanisms of ion permeation and selectivity in ion channels, the relationship between the molecular structure and the physiological function of channels, such as those of the inhibitory neurotransmitter receptor glycine channel and the olfactory cyclic nucleotide-gated channel, and investigating the factors that determine their ion permeation, selectivity and conductance. (edu.au)
  • NE-stimulated cAMP concentration and L-type calcium current were also attenuated by adenoviral nNOS, along with the chronotropic responsiveness to NE in hypertensive rat atria. (ox.ac.uk)
  • Channel activity was enhanced by the presence of the dihydropyridine agonist (+)-202-791 (0.5 microM) and the activated alpha subunit of the stimulatory GTP-binding protein, Gs. (aspetjournals.org)
  • A competitive antagonist will attach itself to the same binding site of the receptor that the agonist will bind to. (wikipedia.org)
  • We found that 0.3-30 microM ethaverine on either side of the channel caused a reduction in the channel open probability (EC50 approximately 1 microM), with the higher concentrations inhibiting channel activity almost completely. (aspetjournals.org)
  • This was accompanied by increased basal and norepinephrine-stimulated L-type calcium current. (ox.ac.uk)
  • For example, in Timothy Syndrome the mutation in the gene produces too much of the protein, in this case the L-type calcium channel Cav1.2. (epiphanyasd.com)
  • L-type calcium channels were activated by step depolarizations from a holding potential of -60 mV to a test potential of 0 mV, and unitary currents carried by 100 mM BaCl2 were recorded. (aspetjournals.org)
  • In both cell lines, the T149A mutant displayed similar agonist affinities as the wild-type receptor. (aspetjournals.org)
  • Calcium (Ca 2 + ) is an important ubiquitous second messenger, involved in the regulation of a diverse range of cellular processes, including cell proliferation, gene transcription, muscle contraction, and endocytosis. (abcam.com)
  • 1 As one major target of volatile anesthetics in the heart, the L-type Ca 2+ channel, responsible for the L-type Ca 2+ current (I Ca,L ), has been identified. (asahq.org)
  • Amlodipine blocks L type channels and N type channels. (epiphanyasd.com)
  • You can both turn on self-injury via activating L type calcium channels and extinguish it by blocking the same channels. (epiphanyasd.com)
  • Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). (pharmfair.com)
  • To some extent Verapamil, Amlodipine and Nicardipine all block P channels. (epiphanyasd.com)
  • In conclusion, the knowledge gained in this study by elucidating the role of calcium in MSC mechanotransduction processes, and that in prolonged stretching results in non-apoptosis mediated cell death may be potential useful for regenerative medicine applications. (um.edu.my)
  • In order to establish this, we disrupted calcium signalling by blocking stretch-activated calcium channel (SACC) in human MSCs (hMSCs) in vitro. (um.edu.my)
  • Actions of anesthetics on ion channels are usually studied in vitro at room temperature. (asahq.org)
  • Calcium deficiency also may increase lead absorption, based on studies in children. (cdc.gov)
  • Coadministration of calcium with lead decreases lead absorption in adults, and in animal studies. (cdc.gov)