Calcium Channel Agonists: 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.Calcium Channel Blockers: A class of drugs that act by selective inhibition of calcium influx through cellular membranes.Calcium Channels: 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.Nitrendipine: 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.Isradipine: 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.Dihydropyridines: Pyridine moieties which are partially saturated by the addition of two hydrogen atoms in any position.Calcium Channels, L-Type: 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.Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.Calcium: 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.Ion Channels: 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.Sodium Channel Agonists: A class of drugs that stimulate sodium influx through cell membrane channels.Calcium Channels, N-Type: CALCIUM CHANNELS that are concentrated in neural tissue. Omega toxins inhibit the actions of these channels by altering their voltage dependence.Calcium Channels, T-Type: 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.Calcium Signaling: 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.Ion Channel Gating: 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.Voltage-Gated Sodium Channel Agonists: Compounds that either stimulate the opening or prevent closure of VOLTAGE-GATED SODIUM CHANNELS.Potassium Channel Blockers: 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.KATP Channels: 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.Diltiazem: A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of CALCIUM ion on membrane functions.Potassium Channels, Inwardly Rectifying: Potassium channels where the flow of K+ ions into the cell is greater than the outward flow.Calcium Channels, P-Type: CALCIUM CHANNELS located within the PURKINJE CELLS of the cerebellum. They are involved in stimulation-secretion coupling of neurons.Calcium Channels, Q-Type: CALCIUM CHANNELS located in the neurons of the brain.Electrophysiology: 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.Nimodipine: A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure.Verapamil: A calcium channel blocker that is a class IV anti-arrhythmia agent.Membrane Potentials: 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, R-Type: CALCIUM CHANNELS located in the neurons of the brain. They are inhibited by the marine snail toxin, omega conotoxin MVIIC.Patch-Clamp Techniques: 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.Chloride Channels: Cell membrane glycoproteins that form channels to selectively pass chloride ions. Nonselective blockers include FENAMATES; ETHACRYNIC ACID; and TAMOXIFEN.Pinacidil: 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)Rats, Sprague-Dawley: 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, Cultured: 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.Barium: 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.omega-Conotoxin GVIA: 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.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Electric Conductivity: The ability of a substrate to allow the passage of ELECTRONS.Calcium, Dietary: 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.Kinetics: The rate dynamics in chemical or physical systems.Epithelial Sodium Channel Agonists: Compounds that either stimulate the opening or prevent closure of EPITHELIAL SODIUM ION CHANNELS.omega-Conotoxins: 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.Neurons: 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 Channels, Voltage-Gated: 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.Potassium: 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, Calcium-Activated: Potassium channels whose activation is dependent on intracellular calcium concentrations.Glyburide: An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.Action Potentials: Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.Nicorandil: 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.Cromakalim: 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)Mibefradil: A benzimidazoyl-substituted tetraline that selectively binds and inhibits CALCIUM CHANNELS, T-TYPE.Sodium Channel Blockers: 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.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Myocardium: 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.Lambert-Eaton Myasthenic Syndrome: 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)Pyrroles: Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.TRPC Cation Channels: 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.omega-Agatoxin IVA: 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.Veratridine: A benzoate-cevane found in VERATRUM and Schoenocaulon. It activates SODIUM CHANNELS to stay open longer than normal.Shaker Superfamily of Potassium Channels: 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.Rabbits: 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.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Dopamine Agonists: Drugs that bind to and activate dopamine receptors.Potassium Chloride: 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.Heart: The hollow, muscular organ that maintains the circulation of the blood.Adenosine Triphosphate: 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.Large-Conductance Calcium-Activated Potassium Channels: 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.Molecular Sequence Data: 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.Benzopyrans: Compounds with a core of fused benzo-pyran rings.Electric Stimulation: Use of electric potential or currents to elicit biological responses.Amino Acid Sequence: 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.Oocytes: 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).Guinea Pigs: 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.TRPV Cation Channels: 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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Calcium Carbonate: 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.Xenopus laevis: 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.Cyclic Nucleotide-Gated Cation Channels: 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.Calcium Chloride: A salt used to replenish calcium levels, as an acid-producing diuretic, and as an antidote for magnesium poisoning.Potassium Channels: 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.Myocardial Contraction: Contractile activity of the MYOCARDIUM.Nicardipine: 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.Muscle, Smooth, Vascular: The nonstriated involuntary muscle tissue of blood vessels.Ryanodine Receptor Calcium Release Channel: 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.Ryanodine: 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.TRPM Cation Channels: 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.Spider Venoms: 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.Muscle Contraction: 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.Acid Sensing Ion Channels: 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)

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The use of TIR-FM enabled us to visualize the steady state and calcium-induced submembrane movement, docking, and fusion of intracellular compartments to the plasma membrane. We found that calcium ionophore A23187 induced increase in calcium did not cause exocytosis of Golgi, ER, early, or late endosomes, and did not lead to an increase in exocytosis of post-Golgi vesicles. The absence of an effect of calcium on exocytosis of early endosomes is in agreement with the previously reported absence of an affect of calcium increase on transferrin recycling (Rodriguez et al., 1997). On the other hand, absence of an effect of calcium on exocytosis of Golgi and Golgi-derived vesicles is contrary to the proposed role of Golgi derived compartments in Ca2+-induced exocytosis in fibroblasts (Togo et al., 1999).. An increase in calcium caused either by the calcium ionophore A23187 or by the IP3-dependent calcium channel agonists thrombin and bombesin, led to exocytosis of lysosomes. Using dual-color live-cell ...
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Calcimimetic Agents (1) • Small organic molecules that act as allosteric activators of the calcium sensing receptor (CaSR) in the PARATHYROID GLANDS and other tissues. They lower the threshold for CaSR activation by extracellular calcium ions and diminish PARATHYROID HORMONE (PTH) release from parathyroid cells. MeSH. Calcineurin Inhibitors (4) • Compounds that inhibit or block the PHOSPHATASE activity of CALCINEURIN. MeSH. Calcium Antagonists, Exogenous (0) see Calcium Channel Blockers. Calcium Channel Agonists (8) • 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. MeSH. Calcium Channel Blockers (117) • A ...
Voltage-dependent calcium channels represent a major pathway of calcium entry into neurons, where they participate actively to cell excitability and to the molecular processes of synaptic transmission. For that reason, they have been the direct or indirect pharmacological targets of analgesics and this long before their implication in the physiology of nociception had been demonstrated. These last years, the still more refined molecular characterization of these channels and their associated regulatory subunits and the demonstration of their implication in nociceptive processes indicates that these structures are prime pharmacological targets for the management of pain. Herein, we detail the recent breakthroughs on calcium channel structure, function and pharmacology, review the implication of calcium channels in the transmission of nociception, and evaluate their importance as targets for the treatment of pain perception. The search for specific inhibitors of voltage-dependent calcium channels appears
TY - JOUR. T1 - Expression of intermediate-conductance, Ca2+-activated K+ channel (KCNN4) in H441 human distal airway epithelial cells. AU - Wilson, Stuart M.. AU - Brown, Sean G.. AU - McTavish, Niall. AU - McNeill, R. P.. AU - Husband, E. M.. AU - Inglis, Sarah K.. AU - Olver, Richard E.. AU - Clunes, M. T.. PY - 2006/6/9. Y1 - 2006/6/9. N2 - Electrophysiological studies of H441 human distal airway epithelial cells showed that thapsigargin caused a Ca2+-dependent increase in membrane conductance (GTot) and hyperpolarization of membrane potential (Vm). These effects reflected a rapid rise in cellular K+ conductance (GK) and a slow fall in amiloride-sensitive Na+ conductance (GNa). The increase in GTot was antagonized by Ba2+, a nonselective K+ channel blocker, and abolished by clotrimazole, a KCNN4 inhibitor, but unaffected by other selective K+ channel blockers. Moreover, 1-ethyl-2-benzimidazolinone (1-EBIO), which is known to activate KCNN4, increased GK with no effect on GNa. RT-PCR-based ...
TY - JOUR. T1 - Domain III regulates N-type (Ca V2.2) calcium channel closing kinetics. AU - Yarotskyy, Viktor. AU - Gao, Guofeng. AU - Peterson, Blaise Z.. AU - Elmslie, Keith S.. PY - 2012/4/1. Y1 - 2012/4/1. N2 - Ca V2.2 (N-type) and Ca V1.2 (L-type) calcium channels gate differently in response to membrane depolarization, which is critical to the unique physiological functions mediated by these channels. We wondered if the source for these differences could be identified. As a first step, we examined the effect of domain exchange between N-type and L-type channels on activationdeactivation kinetics, which were significantly different between these channels. Kinetic analysis of chimeric channels revealed N-channellike deactivation for all chimeric channels containing N-channel domain III, while activation appeared to be a more distributed function across domains. This led us to hypothesize that domain III was an important regulator of N-channel closing. This idea was further examined with ...
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As Morse code enables information to be transmitted as a series of on-off tones and clicks, which can be decoded into words and text, in a somewhat similar manner, calcium (Ca2+) signals are encoded as distinct patterns of input with varying amplitudes, frequencies, and durations. As (Ca2+) is involved in literally every single cellular process in our body, it has been tempting to manipulate intracellular (Ca2+) levels for research or therapeutic purposes.. Recently, in high profile work, researchers have succeeded in developing a blue-light-dependent endogenous (Ca2+) channel activator, named OptoSTIM1 (an optically activated STIM1 protein). In this work, a light-responsive oligomerization plant protein, Cryptochrome2, was conjugated with a (Ca2+) channel activator, STIM1, which binds to (Ca2+) channels only when oligomerized by themselves. Depending on the power and exposure time of blue-light, (Ca2+) levels in the cell could be quantitatively controlled; varied levels of (Ca2+) could be ...
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1988). "Some Chemical Properties of Maitotoxin, a Putative Calcium Channel Agonist Isolated from a Marine Dinoflagellate". J. ... Maitotoxin activates extracellular calcium channels, leading to an increase in levels of cytosolic Ca2+ ions. It is thought ... Maitotoxin can indirectly activate calcium-binding proteases calpain-1 and calpain-2, contributing to necrosis. The toxicity of ... that maitotoxin leads to the formation of pores on these ion channels. Ultimately, a cell death cascade is activated, resulting ...
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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/ ...
... calcium channel agonists MeSH D27.505.519.562.249 --- calcium channel blockers MeSH D27.505.519.562.374 --- ionophores MeSH ... calcium channel agonists MeSH D27.505.954.411.793.610 --- nasal decongestants MeSH D27.505.954.411.918 --- vasodilator agents ... calcium channel blockers MeSH D27.505.954.411.207 --- cardioplegic solutions MeSH D27.505.954.411.222 --- cardiotonic agents ... adrenergic alpha-agonists MeSH D27.505.519.625.050.100.200 --- adrenergic beta-agonists MeSH D27.505.519.625.050.200 --- ...
... is a GABA-A receptor agonist action and may affect sodium channels and voltage-sensitive calcium channels. Like other ... GABA Receptor Agonists". Drugs and Diseases. Medccape. Retrieved 10 July 2005. Ralvenius WT, Acuña MA, Benke D, Matthey A, ... channels. It was also reported that these effects were inhibited by the GABA antagonist flumazenil, and that clobazam acts more ...
Acetylcholine Digoxin The non-dihydropyridine calcium channel blockers diltiazem and verapamil Most Adrenergic agonists ...
In addition, β2 agonists open large conductance calcium-activated potassium channels and thereby tend to hyperpolarize airway ... β2 (beta2) adrenergic receptor agonists, also known as adrenergic β2 receptor agonists, are a class of drugs that act on the β2 ... Discovery and development of β2 agonists Ramanujan K. Common beta-agonist inhalers more than double death rate in COPD patients ... Like other β adrenergic agonists, they cause smooth muscle relaxation. β2 adrenergic agonists' effects on smooth muscle cause ...
β1 agonists stimulate adenylyl cyclase activity and opening of calcium channel (cardiac stimulants; used to treat cardiogenic ... β2 agonists stimulate adenylyl cyclase activity and closing of calcium channel (smooth muscle relaxants; used to treat asthma ... Beta adrenergic agonists or beta agonists are medications that relax muscles of the airways, which widen the airways and result ... In general, pure beta-adrenergic agonists have the opposite function of beta blockers. Beta adrenoreceptor agonist ligands ...
... 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 airway smooth muscles to relax. Salbutamol was first ... There is no compelling evidence that salbutamol and other β2 agonists can increase performance in healthy athletes. In spite of ...
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 ...
... which is responsible for turning on calcium inflow channels. A decrease in activation of calcium channels will therefore result ... beta2-adrenergic agonists, and clonidine. Some evidence suggests that sotalol should be avoided in the setting of heart failure ... 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, ...
A more recent example is the N-type calcium channel blocker ziconotide analgesic which is based on a cyclic peptide cone snail ... The most potent narcotic component of opium is the alkaloid morphine which acts as an opioid receptor agonist. ... an N-type neuronal calcium channel blocker found in the venom of Conus magus". Toxicon. 36 (11): 1651-8. doi:10.1016/S0041-0101 ... ion channels, and enzymes. In some cases, they have also served as leads in the development of novel drugs. For example, ...
The activation of the potassium channel and subsequent deactivation of the calcium channel causes membrane hyperpolarization. ... such as the μ agonist etorphine and the κ agonist bremazocine, have been shown to act as agonists for this effect (even in the ... Voltage-gated dependent calcium channel, (VDCCs), are key in the depolarisation of neurons, and play a major role in promoting ... When the sub-unit binds to the voltage-dependent calcium channel, it produces a voltage-dependant block, which inhibits the ...
They found that charged sodium-channel blockers can be targeted into nociceptors by the application of TRPV1 agonists to ... Voltage sensing in thermo-TRP channels has been reviewed by Brauchi et al. TRP channels have six TMS helices. These channels ... 2F37​ Transient receptor potential cation channel subfamily A member 1: PDB: 3J9P​ Voltage-gated ion channel Ion channel ... The transient receptor potential Ca2+ channel (TRP-CC) family (TC# 1.A.4) is a member of the voltage-gated ion channel (VIC) ...
The drug also dose-dependently blocks voltage-gated calcium channels. It is not a benzodiazepine; instead, it is an imidazolone ... a full agonist of this site). It is the first partial agonist to be approved for the treatment of epilepsy. ... partial agonist of the benzodiazepine site of the GABAA receptor (up to 12-21% of the maximal potentiation of diazepam, ... the first partial benzodiazepine receptor agonist developed for the treatment of epilepsy". CNS Drugs. 28 (1): 29-43. doi: ...
Other research has also suggested that calcium flow through N-type calcium channels is essential for normal breathing, and is ... Several synthetic compounds have been shown to act on neurons specific to the preBötC, most being selective agonists or ... Other potassium channels like large conductance calcium-dependent potassium channels and sodium chloride dependent potassium ... voltage gated calcium channels become activated and calcium is able to flow into the cell which usually leads to the release of ...
Direct observation of the agonist specific regional vulnerability to glutamate, NMDA and kainate neurotoxicity in organotypic ... Second, if calcium entry through N-type calcium channels is prevented, the delayed generation of damage is prevented. ... that neuroprotection by selective N-type calcium channel antagonists is mediated directly through neuronal calcium channels. In ... Pharmacological characterisation of the calcium channels coupled to the plateau phase of KCl-induced free calcium elevated in ...
  • In addition, the enhancing effects of BK Ca channel blockers tetraethylammonium (TEA) and paxilline on action potential firing were sensitive to resveratrol. (biomedcentral.com)
  • Moreover, the action potential firing rates evoked by the depolarizing current and BK Ca channel blockers were remarkably decreased by application of resveratrol. (biomedcentral.com)
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