One of the POTASSIUM CHANNEL BLOCKERS, with secondary effect on calcium currents, which is used mainly as a research tool and to characterize channel subtypes.
Pyridines substituted in any position with an amino group. May be hydrogenated, but must retain at least one double bond.
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.
A potassium-selective ion channel blocker. (From J Gen Phys 1994;104(1):173-90)
Tetraethylammonium compounds refer to a group of organic salts containing the tetraethylammonium ion (N(C2H5)4+), which is characterized by four ethyl groups bonded to a central nitrogen atom, and are commonly used in research and medicine as pharmacological tools for studying ion 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.
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).
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.
A 37-amino acid residue peptide isolated from the scorpion Leiurus quinquestriatus hebraeus. It is a neurotoxin that inhibits calcium activated potassium channels.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
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.
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 group of slow opening and closing voltage-gated potassium channels. Because of their delayed activation kinetics they play an important role in controlling ACTION POTENTIAL duration.
A delayed rectifier subtype of shaker potassium channels that conducts a delayed rectifier current. It contributes to ACTION POTENTIAL repolarization of MYOCYTES in HEART ATRIA.
Venoms from snakes of the family Elapidae, including cobras, kraits, mambas, coral, tiger, and Australian snakes. The venoms contain polypeptide toxins of various kinds, cytolytic, hemolytic, and neurotoxic factors, but fewer enzymes than viper or crotalid venoms. Many of the toxins have been characterized.
Inorganic compounds that contain barium as an integral part of the molecule.
Drugs that interrupt transmission at the skeletal neuromuscular junction by causing sustained depolarization of the motor end plate. These agents are primarily used as adjuvants in surgical anesthesia to cause skeletal muscle relaxation.
A highly neurotoxic polypeptide from the venom of the honey bee (Apis mellifera). It consists of 18 amino acids with two disulfide bridges and causes hyperexcitability resulting in convulsions and respiratory paralysis.
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.
An aminoperhydroquinazoline poison found mainly in the liver and ovaries of fishes in the order TETRAODONTIFORMES, which are eaten. The toxin causes paresthesia and paralysis through interference with neuromuscular conduction.
The ability of a substrate to allow the passage of ELECTRONS.
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.
A member of the alkali metals. It has an atomic symbol Cs, atomic number 50, and atomic weight 132.91. Cesium has many industrial applications, including the construction of atomic clocks based on its atomic vibrational frequency.
An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.
An optical isomer of quinine, extracted from the bark of the CHINCHONA tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular ACTION POTENTIALS, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission.
Potassium channels whose activation is dependent on intracellular calcium concentrations.
A fast inactivating subtype of shaker potassium channels that contains two inactivation domains at its N terminus.
Venoms from animals of the order Scorpionida of the class Arachnida. They contain neuro- and hemotoxins, enzymes, and various other factors that may release acetylcholine and catecholamines from nerve endings. Of the several protein toxins that have been characterized, most are immunogenic.
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.
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 shaker subfamily that is prominently expressed in NEURONS and are necessary for high-frequency, repetitive firing of ACTION POTENTIALS.
Use of electric potential or currents to elicit biological responses.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
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.
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.
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.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
An alkaloid derived from the bark of the cinchona tree. It is used as an antimalarial drug, and is the active ingredient in extracts of the cinchona that have been used for that purpose since before 1633. Quinine is also a mild antipyretic and analgesic and has been used in common cold preparations for that purpose. It was used commonly and as a bitter and flavoring agent, and is still useful for the treatment of babesiosis. Quinine is also useful in some muscular disorders, especially nocturnal leg cramps and myotonia congenita, because of its direct effects on muscle membrane and sodium channels. The mechanisms of its antimalarial effects are not well understood.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A delayed rectifier subtype of shaker potassium channels that is commonly mutated in human episodic ATAXIA and MYOKYMIA.
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
A subfamily of shaker potassium channels that shares homology with its founding member, Shab protein, Drosophila. They regulate delayed rectifier currents in the NERVOUS SYSTEM of DROSOPHILA and in the SKELETAL MUSCLE and HEART of VERTEBRATES.
A delayed rectifier subtype of shaker potassium channels that is selectively inhibited by a variety of SCORPION VENOMS.
Paracrine substances produced by the VASCULAR ENDOTHELIUM with VASCULAR SMOOTH MUSCLE relaxation (VASODILATION) activities. Several factors have been identified, including NITRIC OXIDE and PROSTACYCLIN.
The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.
The nonstriated involuntary muscle tissue of blood vessels.
Substances that act in the brain stem or spinal cord to produce tonic or clonic convulsions, often by removing normal inhibitory tone. They were formerly used to stimulate respiration or as antidotes to barbiturate overdose. They are now most commonly used as experimental tools.
A cholinesterase inhibitor with a slightly longer duration of action than NEOSTIGMINE. It is used in the treatment of myasthenia gravis and to reverse the actions of muscle relaxants.
The sequence of carbohydrates within POLYSACCHARIDES; GLYCOPROTEINS; and GLYCOLIPIDS.
Electrodes with an extremely small tip, used in a voltage clamp or other apparatus to stimulate or record bioelectric potentials of single cells intracellularly or extracellularly. (Dorland, 28th ed)
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.
A neuromuscular blocker and active ingredient in CURARE; plant based alkaloid of Menispermaceae.
A shaker subfamily of potassium channels that participate in transient outward potassium currents by activating at subthreshold MEMBRANE POTENTIALS, inactivating rapidly, and recovering from inactivation quickly.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
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)
That phase of a muscle twitch during which a muscle returns to a resting position.
A local anesthetic of the ester type that has a slow onset and a short duration of action. It is mainly used for infiltration anesthesia, peripheral nerve block, and spinal block. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1016).
Quinoxalines are heterocyclic organic compounds consisting of a benzene fused to a pyrazine ring, which have been studied for their potential antibacterial, antifungal, and anticancer properties.
Stretch receptors found in the bronchi and bronchioles. Pulmonary stretch receptors are sensors for a reflex which stops inspiration. In humans, the reflex is protective and is probably not activated during normal respiration.
An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to CADMIUM POISONING.
Electrical responses recorded from nerve, muscle, SENSORY RECEPTOR, or area of the CENTRAL NERVOUS SYSTEM following stimulation. They range from less than a microvolt to several microvolts. The evoked potential can be auditory (EVOKED POTENTIALS, AUDITORY), somatosensory (EVOKED POTENTIALS, SOMATOSENSORY), visual (EVOKED POTENTIALS, VISUAL), or motor (EVOKED POTENTIALS, MOTOR), or other modalities that have been reported.
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.
The synapse between a neuron and a muscle.
Potassium channels that contain two pores in tandem. They are responsible for baseline or leak currents and may be the most numerous of all K channels.
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)
Projection neurons in the CEREBRAL CORTEX and the HIPPOCAMPUS. Pyramidal cells have a pyramid-shaped soma with the apex and an apical dendrite pointed toward the pial surface and other dendrites and an axon emerging from the base. The axons may have local collaterals but also project outside their cortical region.
Basic lipopeptide antibiotic group obtained from Bacillus polymyxa. They affect the cell membrane by detergent action and may cause neuromuscular and kidney damage. At least eleven different members of the polymyxin group have been identified, each designated by a letter.
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.
The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.
Drugs used to cause dilation of the blood vessels.
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.
The rate dynamics in chemical or physical systems.
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.
Branch-like terminations of NERVE FIBERS, sensory or motor NEURONS. Endings of sensory neurons are the beginnings of afferent pathway to the CENTRAL NERVOUS SYSTEM. Endings of motor neurons are the terminals of axons at the muscle cells. Nerve endings which release neurotransmitters are called PRESYNAPTIC TERMINALS.
A calcium channel blocker that is a class IV anti-arrhythmia agent.
The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation.
A molluscan neuroactive peptide which induces a fast excitatory depolarizing response due to direct activation of amiloride-sensitive SODIUM CHANNELS. (From Nature 1995; 378(6558): 730-3)
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 potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
The hollow, muscular organ that maintains the circulation of the blood.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or "seizure disorder."
The hemodynamic and electrophysiological action of the HEART VENTRICLES.
Elements of limited time intervals, contributing to particular results or situations.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
Substances used for their pharmacological actions on any aspect of neurotransmitter systems. Neurotransmitter agents include agonists, antagonists, degradation inhibitors, uptake inhibitors, depleters, precursors, and modulators of receptor function.
An agent derived from licorice root. It is used for the treatment of digestive tract ulcers, especially in the stomach. Antidiuretic side effects are frequent, but otherwise the drug is low in toxicity.
A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)
Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.
Oxadiazoles are heterocyclic organic compounds consisting of a five-membered ring containing two carbon atoms, one nitrogen atom, and two oxygen atoms (one as a part of the oxadiazole ring and the other as a substituent or part of a larger molecule), which can exist in various isomeric forms and are known for their versatile biological activities, including anti-inflammatory, antiviral, antibacterial, and antitumor properties.
An isoquinoline alkaloid obtained from Dicentra cucullaria and other plants. It is a competitive antagonist for GABA-A receptors.
The characteristic 3-dimensional shape of a carbohydrate.
Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)

Characterization of K+ currents underlying pacemaker potentials of fish gonadotropin-releasing hormone cells. (1/1089)

Endogenous pacemaker activities are important for the putative neuromodulator functions of the gonadotropin-releasing hormone (GnRH)-immunoreactive terminal nerve (TN) cells. We analyzed several types of voltage-dependent K+ currents to investigate the ionic mechanisms underlying the repolarizing phase of pacemaker potentials of TN-GnRH cells by using the whole brain in vitro preparation of fish (dwarf gourami, Colisa lalia). TN-GnRH cells have at least four types of voltage-dependent K+ currents: 1) 4-aminopyridine (4AP)-sensitive K+ current, 2) tetraethylammonium (TEA)-sensitive K+ current, and 3) and 4) two types of TEA- and 4AP-resistant K+ currents. A transient, low-threshold K+ current, which was 4AP sensitive and showed significant steady-state inactivation in the physiological membrane potential range (-40 to -60 mV), was evoked from a holding potential of -100 mV. This current thus cannot contribute to the repolarizing phase of pacemaker potentials. TEA-sensitive K+ current evoked from a holding potential of -100 mV was slowly activating, long lasting, and showed comparatively low threshold of activation. This current was only partially inactivated at steady state of -60 to -40 mV, which is equivalent to the resting membrane potential. TEA- and 4AP-resistant sustained K+ currents were evoked from a holding potential of -100 mV and were suggested to consist of two types, based on the analysis of activation curves. From the inactivation and activation curves, it was suggested that one of them with low threshold of activation may be partly involved in the repolarizing phase of pacemaker potentials. Bath application of TEA together with tetrodotoxin reversibly blocked the pacemaker potentials in current-clamp recordings. We conclude that the TEA-sensitive K+ current is the most likely candidate that contributes to the repolarizing phase of the pacemaker potentials of TN-GnRH cells.  (+info)

Presynaptic action of adenosine on a 4-aminopyridine-sensitive current in the rat carotid body. (2/1089)

1. Plasma adenosine concentration increases during hypoxia to a level that excites carotid body chemoreceptors by an undetermined mechanism. We have examined this further by determining the electrophysiological responses to exogenous adenosine of sinus nerve chemoafferents in vitro and of whole-cell currents in isolated type I cells. 2. Steady-state, single-fibre chemoafferent discharge was increased approximately 5-fold above basal levels by 100 microM adenosine. This adenosine-stimulated discharge was reversibly and increasingly reduced by methoxyverapamil (D600, 100 microM), by application of nickel chloride (Ni2+, 2 mM) and by removal of extracellular Ca2+. These effects strongly suggest a presynaptic, excitatory action of adenosine on type I cells of the carotid body. 3. Adenosine decreased whole-cell outward currents at membrane potentials above -40 mV in isolated type I cells recorded during superfusion with bicarbonate-buffered saline solution at 34-36 C. This effect was reversible and concentration dependent with a maximal effect at 10 microM. 4. The degree of current inhibition induced by 10 microM adenosine was voltage independent (45.39 +/- 2. 55 % (mean +/- s.e.m.) between -40 and +30 mV) and largely ( approximately 75 %), but not entirely, Ca2+ independent. 4-Aminopyridine (4-AP, 5 mM) decreased the amplitude of the control outward current by 80.60 +/- 3.67 % and abolished the effect of adenosine. 5. Adenosine was without effect upon currents near the resting membrane potential of approximately -55 mV and did not induce depolarization in current-clamp experiments. 6. We conclude that adenosine acts to inhibit a 4-AP-sensitive current in isolated type I cells of the rat carotid body and suggest that this mechanism contributes to the chemoexcitatory effect of adenosine in the whole carotid body.  (+info)

Contribution of delayed rectifier potassium currents to the electrical activity of murine colonic smooth muscle. (3/1089)

1. We used intracellular microelectrodes to record the membrane potential (Vm) of intact murine colonic smooth muscle. Electrical activity consisted of spike complexes separated by quiescent periods (Vm approximately -60 mV). The spike complexes consisted of about a dozen action potentials of approximately 30 mV amplitude. Tetraethylammonium (TEA, 1-10 mM) had little effect on the quiescent periods but increased the amplitude of the action potential spikes. 4-Aminopyridine (4-AP, >= 5 mM) caused continuous spiking. 2. Voltage clamp of isolated myocytes identified delayed rectifier K+ currents that activated rapidly (time to half-maximum current, 11.5 ms at 0 mV) and inactivated in two phases (tauf = 96 ms, taus = 1.5 s at 0 mV). The half-activation voltage of the permeability was -27 mV, with significant activation at -50 mV. 3. TEA (10 mM) reduced the outward current at potentials positive to 0 mV. 4-AP (5 mM) reduced the early current but increased outward current at later times (100-500 ms) consistent with block of resting channels relieved by depolarization. 4-AP inhibited outward current at potentials negative to -20 mV, potentials where TEA had no effect. 4. Qualitative PCR amplification of mRNA identified transcripts encoding delayed rectifier K+ channel subunits Kv1.6, Kv4.1, Kv4.2, Kv4.3 and the Kvbeta1.1 subunit in murine colon myocytes. mRNA encoding Kv 1.4 was not detected. 5. We find that TEA-sensitive delayed rectifier currents are important determinants of action potential amplitude but not rhythmicity. Delayed rectifier currents sensitive to 4-AP are important determinants of rhythmicity but not action potential amplitude.  (+info)

Calcium responses induced by acetylcholine in submucosal arterioles of the guinea-pig small intestine. (4/1089)

1. Calcium responses induced by brief stimulation with acetylcholine (ACh) were assessed from the fluorescence changes in fura-2 loaded submucosal arterioles of the guinea-pig small intestine. 2. Initially, 1-1.5 h after loading with fura-2 (fresh tissues), ACh increased [Ca2+]i in a concentration-dependent manner. This response diminished with time, and finally disappeared in 2-3 h (old tissues). 3. Ba2+ elevated [Ca2+]i to a similar extent in both fresh and old tissues. ACh further increased the Ba2+-elevated [Ca2+]i in fresh tissues, but reduced it in old tissues. Responses were not affected by either indomethacin or nitroarginine. 4. In fresh mesenteric arteries, mechanical removal of endothelial cells abolished the ACh-induced increase in [Ca2+]i, with no alteration of [Ca2+]i at rest and during elevation with Ba2+. 5. In the presence of indomethacin and nitroarginine, high-K+ solution elevated [Ca2+]i in both fresh and old tissues. Subsequent addition of ACh further increased [Ca2+]i in fresh tissues without changing it in old tissues. 6. Proadifen, an inhibitor of the enzyme cytochrome P450 mono-oxygenase, inhibited the ACh-induced changes in [Ca2+]i in both fresh and Ba2+-stimulated old tissues. It also inhibited the ACh-induced hyperpolarization. 7. In fresh tissues, the ACh-induced Ca2+ response was not changed by apamin, charybdotoxin (CTX), 4-aminopyridine (4-AP) or glibenclamide. In old tissues in which [Ca2+]i had previously been elevated with Ba2+, the ACh-induced Ca2+ response was inhibited by CTX but not by apamin, 4-AP or glibenclamide. 8. It is concluded that in submucosal arterioles, ACh elevates endothelial [Ca2+]i and reduces muscular [Ca2+]i, probably through the hyperpolarization of endothelial or smooth muscle membrane by activating CTX-sensitive K+ channels.  (+info)

Identification and characterization of multiple subtypes of muscarinic acetylcholine receptors and their physiological functions in canine hearts. (5/1089)

M2 receptors have long been believed to be the only functional subtype of muscarinic acetylcholine receptor (mAChR) in the heart, although recent studies have provided evidence for the presence of other subtypes. We performed a detailed study to clarify this issue. In the presence of tetramethylammonium (1 microM to 10 mM), a novel K+ current with both delayed rectifying and inward rectifying properties (IKTMA) was activated in single canine atrial myocytes. 4-Aminopyridine (0.05-2 mM) also induced a K+ current (IK4AP) with characteristics similar to but distinct from those of IKTMA. Both IKTMA and IK4AP were abolished by 1 microM atropine. IK4AP, but not IKTMA, was minimized by treatment with pertussis toxin. IKTMA was markedly decreased by 4-diphenylacetoxy-N-methylpiperidine methiodide (a selective antagonist for M3 subtype) but was not altered by pirenzepine (for M1), methoctramine (for M2), and tropicamide (for M4). Tropicamide substantially reduced IK4AP, but the antagonists for other mAChR subtypes had no effects on IK4AP. By comparison, IKACh (ACh-induced K+ current) was significantly depressed by methoctramine but was unaltered by other antagonists. Results from displacement binding of [methyl-3H]N-scopolamine methyl chloride with pirenzepine, methoctramine, 4-diphenylacetoxy-N-methylpiperidine methiodide, or tropicamide revealed the coexistence of multiple mAChR subtypes in canine atrium. Cloning of cDNA fragments and detection of mRNAs coding for M2, M3, and M4 provided further supporting evidence. Our results suggest that 1) multiple subtypes of mAChRs (M2/M3/M4) coexist in the dog heart and 2) different subtypes of mAChRs are coupled to different K+ channels. Our findings represent the first functional evidence for the physiological role of cardiac M3 and M4 receptors.  (+info)

Transient potassium currents regulate the discharge patterns of dorsal cochlear nucleus pyramidal cells. (6/1089)

Pyramidal cells in the dorsal cochlear nucleus (DCN) show three distinct temporal discharge patterns in response to sound: "pauser," "buildup," and "chopper." Similar discharge patterns are seen in vitro and depend on the voltage from which the cell is depolarized. It has been proposed that an inactivating A-type K+ current (IKI) might play a critical role in generating the three different patterns. In this study we examined the characteristics of transient currents in DCN pyramidal cells to evaluate this hypothesis. Morphologically identified pyramidal cells in rat brain slices (P11-P17) exhibited the three voltage-dependent discharge patterns. Two inactivating currents were present in outside-out patches from pyramidal cells: a rapidly inactivating (IKIF, tau approximately 11 msec) current insensitive to block by tetraethylammonium (TEA) and variably blocked by 4-aminopyridine (4-AP) with half-inactivation near -85 mV, and a slowly inactivating TEA- and 4-AP-sensitive current (IKIS, tau approximately 145 msec) with half-inactivation near -35 mV. Recovery from inactivation at 34 degrees C was described by a single exponential with a time constant of 10-30 msec, similar to the rate at which first spike latency increases with the duration of a hyperpolarizing prepulse. Acutely isolated cells also possessed a rapidly activating (<1 msec at 22 degrees C) transient current that activated near -45 mV and showed half-inactivation near -80 mV. A model demonstrated that the deinactivation of IKIF was correlated with the discharge patterns. Overall, the properties of the fast inactivating K+ current were consistent with their proposed role in shaping the discharge pattern of DCN pyramidal cells.  (+info)

On the mechanism of histaminergic inhibition of glutamate release in the rat dentate gyrus. (7/1089)

1. Histaminergic depression of excitatory synaptic transmission in the rat dentate gyrus was investigated using extracellular and whole-cell patch-clamp recording techniques in vitro. 2. Application of histamine (10 microM, 5 min) depressed synaptic transmission in the dentate gyrus for 1 h. This depression was blocked by the selective antagonist of histamine H3 receptors, thioperamide (10 microM). 3. The magnitude of the depression caused by histamine was inversely related to the extracellular Ca2+ concentration. Application of the N-type calcium channel blocker omega-conotoxin (0. 5 or 1 microM) or the P/Q-type calcium channel blocker omega-agatoxin (800 nM) did not prevent depression of synaptic transmission by histamine. 4. The potassium channel blocker 4-aminopyridine (4-AP, 100 microM) enhanced synaptic transmission and reduced the depressant effect of histamine (10 microM). 4-AP reduced the effect of histamine more in 2 mM extracellular calcium than in 4 mM extracellular calcium. 5. Histamine (10 microM) did not affect the amplitude of miniature excitatory postsynaptic currents (mEPSCs) and had only a small effect on their frequency. 6. Histaminergic depression was not blocked by an inhibitor of serine/threonine protein kinases, H7 (100 microM), or by an inhibitor of tyrosine kinases, Lavendustin A (10 microM). 7. Application of adenosine (20 microM) or the adenosine A1 agonist N6-cyclopentyladenosine (CPA, 0.3 microM) completely occluded the effect of histamine (10 microM). 8. We conclude that histamine, acting on histamine H3 receptors, inhibits glutamate release by inhibiting presynaptic calcium entry, via a direct G-protein-mediated inhibition of multiple calcium channels. Histamine H3 receptors and adenosine A1 receptors act upon a common final effector to cause presynaptic inhibition.  (+info)

The cAMP transduction cascade mediates the PGE2-induced inhibition of potassium currents in rat sensory neurones. (8/1089)

1. The role of the cyclic AMP (cAMP) transduction cascade in mediating the prostaglandin E2 (PGE2)-induced decrease in potassium current (IK) was investigated in isolated embryonic rat sensory neurones using the whole-cell patch-clamp recording technique. 2. Exposure to 100 microM chlorophenylthio-adenosine cyclic 3', 5'-monophosphate (cpt-cAMP) or 1 microM PGE2 caused a slow suppression of the whole-cell IK by 34 and 36 %, respectively (measured after 20 min), without a shift in the voltage dependence of activation for this current. Neither of these agents altered the shape of the voltage-dependent inactivation curve indicating that the suppression of IK did not result from alterations in the inactivation properties. 3. To determine whether the PGE2-mediated suppression of IK depended on activation of the cAMP pathway, cells were exposed to this prostanoid in the presence of the protein kinase A (PKA) inhibitor, PKI. The PGE2-induced suppression of IK was prevented by PKI. In the absence of PGE2, PKI had no significant effect on the magnitude of IK. 4. Results obtained from protocols using different conditioning prepulse voltages indicated that the extent of cpt-cAMP- and PGE2-mediated suppression of IK was independent of the prepulse voltage. The subtraction of control and treated currents revealed that the cpt-cAMP- and PGE2-sensitive currents exhibited little time-dependent inactivation. Taken together, these results suggest that the modulated currents may be delayed rectifier-like IK. 5. Exposure to the inhibitors of IK, tetraethylammonium (TEA) or 4-aminopyridine (4-AP), reduced the control current elicited by a voltage step to +60 mV by 40-50 %. In the presence of 10 mM TEA, treatment with cpt-cAMP did not result in any further inhibition of IK. In contrast, cpt-cAMP reduced IK by an additional 25-30 % in the presence of 1 mM 4-AP. This effect was independent of the conditioning prepulse voltage. 6. These results establish that PGE2 inhibits an outward IK in sensory neurones via activation of PKA and are consistent with the idea that the PGE2-mediated sensitization of sensory neurones results, in part, from an inhibition of delayed rectifier-like IK.  (+info)

4-Aminopyridine is a type of medication that is used to treat symptoms of certain neurological disorders, such as multiple sclerosis or spinal cord injuries. It works by blocking the action of potassium channels in nerve cells, which helps to improve the transmission of nerve impulses and enhance muscle function.

The chemical name for 4-Aminopyridine is 4-AP or fampridine. It is available as a prescription medication in some countries and can be taken orally in the form of tablets or capsules. Common side effects of 4-Aminopyridine include dizziness, lightheadedness, and numbness or tingling sensations in the hands or feet.

It is important to note that 4-Aminopyridine should only be used under the supervision of a healthcare professional, as it can have serious side effects if not used properly.

Aminopyridines are a group of organic compounds that contain an amino group (-NH2) attached to a pyridine ring, which is a six-membered aromatic heterocycle containing one nitrogen atom. Aminopyridines have various pharmacological properties and are used in the treatment of several medical conditions.

The most commonly used aminopyridines in medicine include:

1. 4-Aminopyridine (also known as Fampridine): It is a potassium channel blocker that is used to improve walking ability in patients with multiple sclerosis (MS) and other neurological disorders. It works by increasing the conduction of nerve impulses in demyelinated nerves, thereby improving muscle strength and coordination.
2. 3,4-Diaminopyridine: It is a potassium channel blocker that is used to treat Lambert-Eaton myasthenic syndrome (LEMS), a rare autoimmune disorder characterized by muscle weakness. It works by increasing the release of acetylcholine from nerve endings, thereby improving muscle strength and function.
3. 2-Aminopyridine: It is an experimental drug that has been studied for its potential use in treating various neurological disorders, including MS, Parkinson's disease, and stroke. It works by increasing the release of neurotransmitters from nerve endings, thereby improving neuronal communication.

Like all medications, aminopyridines can have side effects, including gastrointestinal symptoms, headache, dizziness, and in rare cases, seizures. It is important to use these drugs under the supervision of a healthcare provider and follow their dosage instructions carefully.

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.

Tetraethylammonium (TEA) is not typically defined in the context of medical terminology, but rather it is a chemical compound with the formula (C2H5)4N+. It is used in research and development, particularly in the field of electrophysiology where it is used as a blocking agent for certain types of ion channels.

Medically, TEA may be mentioned in the context of its potential toxicity or adverse effects on the human body. Exposure to TEA can cause symptoms such as nausea, vomiting, diarrhea, abdominal pain, headache, dizziness, and confusion. Severe exposure can lead to more serious complications, including seizures, respiratory failure, and cardiac arrest.

Therefore, while Tetraethylammonium is not a medical term per se, it is important for healthcare professionals to be aware of its potential health hazards and take appropriate precautions when handling or working with this compound.

Tetraethylammonium compounds refer to chemical substances that contain the tetraethylammonium cation (N(C2H5)4+). This organic cation is derived from tetraethylammonium hydroxide, which in turn is produced by the reaction of ethyl alcohol with ammonia and then treated with a strong acid.

Tetraethylammonium compounds are used in various biomedical research applications as they can block certain types of ion channels, making them useful for studying neuronal excitability and neurotransmission. However, these compounds have also been associated with toxic effects on the nervous system and other organs, and their use is therefore subject to strict safety regulations.

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.

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.

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.

Charybdotoxin is a neurotoxin that is derived from the venom of the death stalker scorpion (Leiurus quinquestriatus). It specifically binds to and blocks certain types of ion channels called "big potassium" or "BK" channels, which are found in various tissues including smooth muscle, nerve, and endocrine cells. By blocking these channels, charybdotoxin can alter the electrical activity of cells and potentially affect a variety of physiological processes. It is an important tool in basic research for studying the structure and function of BK channels and their role in various diseases.

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.

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.

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.

Delayed rectifier potassium channels are a type of ion channel found in the membrane of excitable cells, such as nerve and muscle cells. They are called "delayed rectifiers" because they activate and allow the flow of potassium ions (K+) out of the cell after a short delay following an action potential, or electrical signal.

These channels play a crucial role in regulating the duration and frequency of action potentials, helping to restore the resting membrane potential of the cell after it has fired. By allowing K+ to flow out of the cell, delayed rectifier potassium channels help to repolarize the membrane and bring it back to its resting state.

There are several different types of delayed rectifier potassium channels, which are classified based on their biophysical and pharmacological properties. These channels are important targets for drugs used to treat a variety of conditions, including cardiac arrhythmias, epilepsy, and psychiatric disorders.

The Kv1.5 potassium channel, also known as KCNA5, is a type of voltage-gated potassium channel that is widely expressed in various tissues, including the heart and blood vessels. It plays a crucial role in regulating electrical excitability and maintaining physiological functions in these tissues.

In the heart, Kv1.5 channels are primarily located in the atria and contribute to the repolarization phase of the cardiac action potential. They help establish the rapid delayed rectifier current (IKr), which is essential for normal atrial electrical activity and maintaining proper heart rhythm. Mutations or dysfunctions in Kv1.5 channels can lead to various cardiac arrhythmias, such as atrial fibrillation.

In blood vessels, Kv1.5 channels are involved in the regulation of vascular tone and blood pressure. They contribute to the hyperpolarization of vascular smooth muscle cells, which leads to vasodilation and decreased peripheral resistance. Dysregulation of Kv1.5 channels has been implicated in several cardiovascular diseases, including hypertension and atherosclerosis.

Overall, Kv1.5 potassium channels are critical for maintaining proper electrical activity in the heart and regulating vascular tone, making them an important target for therapeutic interventions in various cardiovascular disorders.

Elapid venoms are the toxic secretions produced by elapid snakes, a family of venomous snakes that includes cobras, mambas, kraits, and coral snakes. These venoms are primarily composed of neurotoxins, which can cause paralysis and respiratory failure in prey or predators.

Elapid venoms work by targeting the nervous system, disrupting communication between the brain and muscles. This results in muscle weakness, paralysis, and eventually respiratory failure if left untreated. Some elapid venoms also contain hemotoxins, which can cause tissue damage, bleeding, and other systemic effects.

The severity of envenomation by an elapid snake depends on several factors, including the species of snake, the amount of venom injected, the location of the bite, and the size and health of the victim. Prompt medical treatment is essential in cases of elapid envenomation, as the effects of the venom can progress rapidly and lead to serious complications or death if left untreated.

Barium compounds are inorganic substances that contain the metallic element barium (Ba) combined with one or more other elements. Barium is an alkaline earth metal that is highly reactive and toxic in its pure form. However, when bound with other elements to form barium compounds, it can be used safely for various medical and industrial purposes.

In medicine, barium compounds are commonly used as a contrast material for X-ray examinations of the digestive system. When a patient swallows a preparation containing barium sulfate, the dense compound coats the lining of the esophagus, stomach, and intestines, making them visible on an X-ray image. This allows doctors to diagnose conditions such as ulcers, tumors, or blockages in the digestive tract.

Other barium compounds include barium carbonate, barium chloride, and barium hydroxide, which are used in various industrial applications such as drilling muds, flame retardants, and pigments for paints and plastics. However, these compounds can be toxic if ingested or inhaled, so they must be handled with care.

Neuromuscular depolarizing agents are a type of muscle relaxant used in anesthesia and critical care medicine. These drugs work by causing depolarization of the post-synaptic membrane at the neuromuscular junction, which is the site where nerve impulses are transmitted to muscles. This results in the binding of the drug to the receptor and the activation of ion channels, leading to muscle contraction.

The most commonly used depolarizing agent is suxamethonium (also known as succinylcholine), which has a rapid onset and short duration of action. It is often used during rapid sequence intubation, where there is a need for immediate muscle relaxation to facilitate endotracheal intubation.

However, the use of depolarizing agents can also lead to several side effects, including increased potassium levels in the blood (hyperkalemia), muscle fasciculations, and an increase in intracranial and intraocular pressure. Therefore, these drugs should be used with caution and only under the close supervision of a trained healthcare provider.

Apamin is a neurotoxin found in the venom of the honeybee (Apis mellifera). It is a small peptide consisting of 18 amino acids and has a molecular weight of approximately 2000 daltons. Apamin is known to selectively block certain types of calcium-activated potassium channels, which are involved in the regulation of neuronal excitability. It has been used in scientific research to study the role of these ion channels in various physiological processes.

Clinically, apamin has been investigated for its potential therapeutic effects in a variety of neurological disorders, such as epilepsy and Parkinson's disease. However, its use as a therapeutic agent is not yet approved by regulatory agencies due to the lack of sufficient clinical evidence and concerns about its potential toxicity.

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.

Tetrodotoxin (TTX) is a potent neurotoxin that is primarily found in certain species of pufferfish, blue-ringed octopuses, and other marine animals. It blocks voltage-gated sodium channels in nerve cell membranes, leading to muscle paralysis and potentially respiratory failure. TTX has no known antidote, and medical treatment focuses on supportive care for symptoms. Exposure can occur through ingestion, inhalation, or skin absorption, depending on the route of toxicity.

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.

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.

Cesium is a chemical element with the symbol "Cs" and atomic number 55. It is a soft, silvery-golden alkali metal that is highly reactive. Cesium is never found in its free state in nature due to its high reactivity. Instead, it is found in minerals such as pollucite.

In the medical field, cesium-137 is a radioactive isotope of cesium that has been used in certain medical treatments and diagnostic procedures. For example, it has been used in the treatment of cancer, particularly in cases where other forms of radiation therapy have not been effective. It can also be used as a source of radiation in brachytherapy, a type of cancer treatment that involves placing radioactive material directly into or near tumors.

However, exposure to high levels of cesium-137 can be harmful and may increase the risk of cancer and other health problems. Therefore, its use in medical treatments is closely regulated and monitored to ensure safety.

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.

Quinidine is a Class IA antiarrhythmic medication that is primarily used to treat and prevent various types of cardiac arrhythmias (abnormal heart rhythms). It works by blocking the rapid sodium channels in the heart, which helps to slow down the conduction of electrical signals within the heart and stabilize its rhythm.

Quinidine is derived from the bark of the Cinchona tree and has been used for centuries as a treatment for malaria. However, its antiarrhythmic properties were discovered later, and it became an important medication in cardiology.

In addition to its use in treating arrhythmias, quinidine may also be used off-label for other indications such as the treatment of nocturnal leg cramps or myasthenia gravis. It is available in various forms, including tablets and injectable solutions.

It's important to note that quinidine has a narrow therapeutic index, meaning that there is only a small difference between an effective dose and a toxic one. Therefore, it must be carefully monitored to ensure that the patient is receiving a safe and effective dose. Common side effects of quinidine include gastrointestinal symptoms such as nausea, vomiting, and diarrhea, as well as visual disturbances, headache, and dizziness. More serious side effects can include QT prolongation, which can lead to dangerous arrhythmias, and hypersensitivity reactions.

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.

The Kv1.4 potassium channel, also known as the KCNA4 channel, is a type of voltage-gated potassium channel that is widely expressed in various tissues, including the heart, brain, and skeletal muscle. It plays a crucial role in regulating electrical excitability and membrane potential in these cells.

The Kv1.4 channel is composed of four α-subunits, each containing six transmembrane domains with a pore-forming region between the fifth and sixth domains. The channel opens in response to depolarization of the membrane potential, allowing potassium ions to flow out of the cell, which helps to repolarize the membrane and terminate the action potential.

In the heart, Kv1.4 channels are expressed in the pacemaker cells of the sinoatrial node and help to regulate the heart rate. In the brain, they are involved in regulating neuronal excitability and neurotransmitter release. In skeletal muscle, Kv1.4 channels contribute to the regulation of membrane potential during muscle contraction and relaxation.

Mutations in the KCNA4 gene, which encodes the Kv1.4 channel, have been associated with various inherited arrhythmia syndromes, including familial atrial fibrillation and progressive conduction disease.

Scorpion venoms are complex mixtures of neurotoxins, enzymes, and other bioactive molecules that are produced by the venom glands of scorpions. These venoms are primarily used for prey immobilization and defense. The neurotoxins found in scorpion venoms can cause a variety of symptoms in humans, including pain, swelling, numbness, and in severe cases, respiratory failure and death.

Scorpion venoms are being studied for their potential medical applications, such as in the development of new pain medications and insecticides. Additionally, some components of scorpion venom have been found to have antimicrobial properties and may be useful in the development of new antibiotics.

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.

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.

Shaw potassium channels, also known as KCNA4 channels, are a type of voltage-gated potassium channel that is encoded by the KCNA4 gene in humans. These channels play a crucial role in regulating the electrical excitability of cells, particularly in the heart and nervous system.

Shaw channels are named after James E. Shaw, who first identified them in 1996. They are composed of four subunits that arrange themselves to form a central pore through which potassium ions can flow. The channels are activated by depolarization of the cell membrane and help to repolarize the membrane during action potentials.

Mutations in the KCNA4 gene have been associated with various cardiac arrhythmias, including familial atrial fibrillation and long QT syndrome type 3. These conditions can cause irregular heart rhythms and may increase the risk of sudden cardiac death. Therefore, understanding the function and regulation of Shaw potassium channels is important for developing therapies to treat these disorders.

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.

"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.

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.

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.

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.

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.

Quinine is defined as a bitter crystalline alkaloid derived from the bark of the Cinchona tree, primarily used in the treatment of malaria and other parasitic diseases. It works by interfering with the reproduction of the malaria parasite within red blood cells. Quinine has also been used historically as a muscle relaxant and analgesic, but its use for these purposes is now limited due to potential serious side effects. In addition, quinine can be found in some beverages like tonic water, where it is present in very small amounts for flavoring purposes.

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.

Kv1.1 potassium channel, also known as KCNA1, is a type of voltage-gated potassium channel that plays a crucial role in the regulation of electrical excitability in neurons and other excitable cells. It is encoded by the KCNA1 gene located on chromosome 12p13.

The Kv1.1 channel is composed of four α-subunits, each containing six transmembrane domains with a pore-forming region between the fifth and sixth domains. These channels are responsible for the rapid repolarization of action potentials in neurons, which helps to control the frequency and pattern of neural activity.

Mutations in the KCNA1 gene have been associated with various neurological disorders, including episodic ataxia type 1 (EA1) and familial hemiplegic migraine (FHM). EA1 is characterized by brief episodes of cerebellar ataxia, myokymia, and neuromyotonia, while FHM is a severe form of migraine with aura that can cause temporary paralysis on one side of the body.

Overall, Kv1.1 potassium channels play an essential role in maintaining normal neural excitability and are critical for proper neurological function.

The hippocampus is a complex, curved formation in the brain that resembles a seahorse (hence its name, from the Greek word "hippos" meaning horse and "kampos" meaning sea monster). It's part of the limbic system and plays crucial roles in the formation of memories, particularly long-term ones.

This region is involved in spatial navigation and cognitive maps, allowing us to recognize locations and remember how to get to them. Additionally, it's one of the first areas affected by Alzheimer's disease, which often results in memory loss as an early symptom.

Anatomically, it consists of two main parts: the Ammon's horn (or cornu ammonis) and the dentate gyrus. These structures are made up of distinct types of neurons that contribute to different aspects of learning and memory.

Shaker-related Kv1.5 potassium channels, also known as "Shab potassium channels," are a type of voltage-gated potassium channel that play a crucial role in regulating the electrical activity of cells, particularly in the heart and nervous system. These channels are named after the Shaker gene in Drosophila melanogaster (fruit flies) where they were first discovered and characterized.

The Kv1.5 channel is composed of four pore-forming α-subunits that assemble to form a tetrameric complex. Each α-subunit contains six transmembrane domains, with the voltage-sensing domain located in the fourth transmembrane segment and the potassium selectivity filter located in the pore region between the fifth and sixth transmembrane segments.

Kv1.5 channels are activated by membrane depolarization and contribute to the repolarization phase of the action potential in cardiac myocytes, helping to maintain the normal rhythm of the heart. In addition, Kv1.5 channels play a role in regulating neuronal excitability and neurotransmitter release in the nervous system.

Mutations in the KCNA5 gene, which encodes the Kv1.5 channel, have been associated with various cardiac arrhythmias, including atrial fibrillation and Brugada syndrome. Pharmacological blockade of Kv1.5 channels has also been shown to have potential therapeutic benefits in the treatment of atrial fibrillation and other cardiovascular disorders.

The Kv1.2 potassium channel is a type of voltage-gated potassium channel that is widely expressed in the nervous system and other tissues. It is composed of four pore-forming α subunits, each of which contains six transmembrane domains and a voltage-sensing domain. These channels play important roles in regulating neuronal excitability, repolarization of action potentials, and controlling neurotransmitter release.

Kv1.2 channels are activated by membrane depolarization and mediate the rapid efflux of potassium ions from cells, which helps to restore the resting membrane potential. They can also be modulated by various intracellular signaling pathways and pharmacological agents, making them targets for therapeutic intervention in a variety of neurological disorders.

Mutations in the KCNA2 gene, which encodes the Kv1.2 channel, have been associated with several human diseases, including episodic ataxia type 1, familial hemiplegic migraine, and spinocerebellar ataxia type 13. These mutations can alter channel function and lead to abnormal neuronal excitability, which may contribute to the symptoms of these disorders.

Endothelium-dependent relaxing factors (EDRFs) are substances that are released by the endothelial cells, which line the interior surface of blood vessels. These factors cause relaxation of the smooth muscle in the vessel wall, leading to vasodilation and an increase in blood flow. One of the most well-known EDRFs is nitric oxide (NO), which is produced from the amino acid L-arginine by the enzyme nitric oxide synthase. Other substances that have been identified as EDRFs include prostacyclin and endothelium-derived hyperpolarizing factor (EDHF). These factors play important roles in the regulation of vascular tone, blood pressure, and inflammation.

Synaptic transmission is the process by which a neuron communicates with another cell, such as another neuron or a muscle cell, across a junction called a synapse. It involves the release of neurotransmitters from the presynaptic terminal of the neuron, which then cross the synaptic cleft and bind to receptors on the postsynaptic cell, leading to changes in the electrical or chemical properties of the target cell. This process is critical for the transmission of signals within the nervous system and for controlling various physiological functions in the body.

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.

Convulsants are substances or agents that can cause seizures or convulsions. These can be medications, toxins, or illnesses that lower the seizure threshold and lead to abnormal electrical activity in the brain, resulting in uncontrolled muscle contractions and relaxation. Examples of convulsants include bromides, strychnine, organophosphate pesticides, certain antibiotics (such as penicillin or cephalosporins), and alcohol withdrawal. It is important to note that some medications used to treat seizures can also have convulsant properties at higher doses or in overdose situations.

Pyridostigmine Bromide is a medication that belongs to the class of drugs known as cholinesterase inhibitors. It is primarily used in the treatment of myasthenia gravis, a neuromuscular disorder characterized by muscle weakness and fatigue.

Pyridostigmine works by blocking the action of acetylcholinesterase, an enzyme that breaks down acetylcholine, a neurotransmitter essential for muscle contraction. By preventing the breakdown of acetylcholine, pyridostigmine helps to increase its levels at the neuromuscular junction, thereby improving muscle strength and function.

The bromide salt form of pyridostigmine is commonly used because it is more soluble in water, which makes it easier to administer orally as a liquid or tablet. The medication's effects typically last for several hours, and its dosage may be adjusted based on the patient's response and any side effects experienced.

Common side effects of pyridostigmine include nausea, vomiting, diarrhea, increased salivation, sweating, and muscle cramps. In some cases, higher doses of the medication can lead to more severe side effects such as respiratory distress, seizures, or cardiac arrhythmias. Therefore, it is essential to monitor patients closely while they are taking pyridostigmine and adjust the dosage as necessary to minimize side effects and optimize treatment outcomes.

A "carbohydrate sequence" refers to the specific arrangement or order of monosaccharides (simple sugars) that make up a carbohydrate molecule, such as a polysaccharide or an oligosaccharide. Carbohydrates are often composed of repeating units of monosaccharides, and the sequence in which these units are arranged can have important implications for the function and properties of the carbohydrate.

For example, in glycoproteins (proteins that contain carbohydrate chains), the specific carbohydrate sequence can affect how the protein is processed and targeted within the cell, as well as its stability and activity. Similarly, in complex carbohydrates like starch or cellulose, the sequence of glucose units can determine whether the molecule is branched or unbranched, which can have implications for its digestibility and other properties.

Therefore, understanding the carbohydrate sequence is an important aspect of studying carbohydrate structure and function in biology and medicine.

A microelectrode is a small electrode with dimensions ranging from several micrometers to a few tens of micrometers in diameter. They are used in various biomedical applications, such as neurophysiological studies, neuromodulation, and brain-computer interfaces. In these applications, microelectrodes serve to record electrical activity from individual or small groups of neurons or deliver electrical stimuli to specific neural structures with high spatial resolution.

Microelectrodes can be fabricated using various materials, including metals (e.g., tungsten, stainless steel, platinum), metal alloys, carbon fibers, and semiconductor materials like silicon. The design of microelectrodes may vary depending on the specific application, with some common types being sharpened metal wires, glass-insulated metal microwires, and silicon-based probes with multiple recording sites.

The development and use of microelectrodes have significantly contributed to our understanding of neural function in health and disease, enabling researchers and clinicians to investigate the underlying mechanisms of neurological disorders and develop novel therapies for conditions such as Parkinson's disease, epilepsy, and hearing loss.

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.

Tubocurarine is a type of neuromuscular blocking agent, specifically a non-depolarizing skeletal muscle relaxant. It works by competitively binding to the nicotinic acetylcholine receptors at the motor endplate, thereby preventing the binding of acetylcholine and inhibiting muscle contraction. Tubocurarine is derived from the South American curare plant and has been used in anesthesia to facilitate intubation and mechanical ventilation during surgery. However, its use has largely been replaced by newer, more selective agents due to its potential for histamine release and cardiovascular effects.

I'm sorry for any confusion, but "Shal Potassium Channels" is not a widely recognized or established medical term in the field of physiology or pharmacology. It seems like there might be a misunderstanding or a typo in the term you're looking for.

If you're referring to " Shaw Potassium Channels," these are a type of voltage-gated potassium channel named after the scientist who first described them, Robert A. Shaw. These channels play crucial roles in various physiological processes, including the regulation of heart rate and excitability of nerve cells.

If you meant to ask about something else or need further clarification, please provide more context or check the spelling, and I'll be happy to help!

Acetylcholine is a neurotransmitter, a type of chemical messenger that transmits signals across a chemical synapse from one neuron (nerve cell) to another "target" neuron, muscle cell, or gland cell. It is involved in both peripheral and central nervous system functions.

In the peripheral nervous system, acetylcholine acts as a neurotransmitter at the neuromuscular junction, where it transmits signals from motor neurons to activate muscles. Acetylcholine also acts as a neurotransmitter in the autonomic nervous system, where it is involved in both the sympathetic and parasympathetic systems.

In the central nervous system, acetylcholine plays a role in learning, memory, attention, and arousal. Disruptions in cholinergic neurotransmission have been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, and myasthenia gravis.

Acetylcholine is synthesized from choline and acetyl-CoA by the enzyme choline acetyltransferase and is stored in vesicles at the presynaptic terminal of the neuron. When a nerve impulse arrives, the vesicles fuse with the presynaptic membrane, releasing acetylcholine into the synapse. The acetylcholine then binds to receptors on the postsynaptic membrane, triggering a response in the target cell. Acetylcholine is subsequently degraded by the enzyme acetylcholinesterase, which terminates its action and allows for signal transduction to be repeated.

Vasodilation is the widening or increase in diameter of blood vessels, particularly the involuntary relaxation of the smooth muscle in the tunica media (middle layer) of the arteriole walls. This results in an increase in blood flow and a decrease in vascular resistance. Vasodilation can occur due to various physiological and pathophysiological stimuli, such as local metabolic demands, neural signals, or pharmacological agents. It plays a crucial role in regulating blood pressure, tissue perfusion, and thermoregulation.

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.

Muscle relaxation, in a medical context, refers to the process of reducing tension and promoting relaxation in the skeletal muscles. This can be achieved through various techniques, including progressive muscle relaxation (PMR), where individuals consciously tense and then release specific muscle groups in a systematic manner.

PMR has been shown to help reduce anxiety, stress, and muscle tightness, and improve overall well-being. It is often used as a complementary therapy in conjunction with other treatments for conditions such as chronic pain, headaches, and insomnia.

Additionally, muscle relaxation can also be facilitated through pharmacological interventions, such as the use of muscle relaxant medications. These drugs work by inhibiting the transmission of signals between nerves and muscles, leading to a reduction in muscle tone and spasticity. They are commonly used to treat conditions such as multiple sclerosis, cerebral palsy, and spinal cord injuries.

Procaine is a local anesthetic drug that is used to reduce the feeling of pain in a specific area of the body. It works by blocking the nerves from transmitting painful sensations to the brain. Procaine is often used during minor surgical procedures, dental work, or when a patient needs to have a wound cleaned or stitched up. It can also be used as a diagnostic tool to help determine the source of pain.

Procaine is administered via injection directly into the area that requires anesthesia. The effects of procaine are relatively short-lived, typically lasting between 30 minutes and two hours, depending on the dose and the individual's metabolism. Procaine may also cause a brief period of heightened sensory perception or euphoria following injection, known as "procaine rush."

It is important to note that procaine should only be administered by trained medical professionals, as improper use can lead to serious complications such as allergic reactions, respiratory depression, and even death.

Quinoxalines are not a medical term, but rather an organic chemical compound. They are a class of heterocyclic aromatic compounds made up of a benzene ring fused to a pyrazine ring. Quinoxalines have no specific medical relevance, but some of their derivatives have been synthesized and used in medicinal chemistry as antibacterial, antifungal, and antiviral agents. They are also used in the production of dyes and pigments.

Pulmonary stretch receptors are nerve endings (receptors) located in the smooth muscle of the airways, specifically within the bronchi and bronchioles of the lungs. They are also known as irritant receptors or slowly adapting receptors. These receptors respond to mechanical deformation caused by lung inflation during breathing. When the lungs stretch, these receptors send signals to the brain via the vagus nerve, which helps regulate breathing patterns and depth. This reflex is known as the Hering-Breuer reflex, which can inhibit inspiration and promote expiration, preventing overinflation of the lungs and helping maintain lung volume within normal ranges.

Cadmium is a toxic heavy metal that is a byproduct of the mining and smelting of zinc, lead, and copper. It has no taste or smell and can be found in small amounts in air, water, and soil. Cadmium can also be found in some foods, such as kidneys, liver, and shellfish.

Exposure to cadmium can cause a range of health effects, including kidney damage, lung disease, fragile bones, and cancer. Cadmium is classified as a known human carcinogen by the International Agency for Research on Cancer (IARC) and the National Toxicology Program (NTP).

Occupational exposure to cadmium can occur in industries that produce or use cadmium, such as battery manufacturing, metal plating, and pigment production. Workers in these industries may be exposed to cadmium through inhalation of cadmium-containing dusts or fumes, or through skin contact with cadmium-containing materials.

The general population can also be exposed to cadmium through the environment, such as by eating contaminated food or breathing secondhand smoke. Smoking is a major source of cadmium exposure for smokers and those exposed to secondhand smoke.

Prevention measures include reducing occupational exposure to cadmium, controlling emissions from industrial sources, and reducing the use of cadmium in consumer products. Regular monitoring of air, water, and soil for cadmium levels can also help identify potential sources of exposure and prevent health effects.

Evoked potentials (EPs) are medical tests that measure the electrical activity in the brain or spinal cord in response to specific sensory stimuli, such as sight, sound, or touch. These tests are often used to help diagnose and monitor conditions that affect the nervous system, such as multiple sclerosis, brainstem tumors, and spinal cord injuries.

There are several types of EPs, including:

1. Visual Evoked Potentials (VEPs): These are used to assess the function of the visual pathway from the eyes to the back of the brain. A patient is typically asked to look at a patterned image or flashing light while electrodes placed on the scalp record the electrical responses.
2. Brainstem Auditory Evoked Potentials (BAEPs): These are used to evaluate the function of the auditory nerve and brainstem. Clicking sounds are presented to one or both ears, and electrodes placed on the scalp measure the response.
3. Somatosensory Evoked Potentials (SSEPs): These are used to assess the function of the peripheral nerves and spinal cord. Small electrical shocks are applied to a nerve at the wrist or ankle, and electrodes placed on the scalp record the response as it travels up the spinal cord to the brain.
4. Motor Evoked Potentials (MEPs): These are used to assess the function of the motor pathways in the brain and spinal cord. A magnetic or electrical stimulus is applied to the brain or spinal cord, and electrodes placed on a muscle measure the response as it travels down the motor pathway.

EPs can help identify abnormalities in the nervous system that may not be apparent through other diagnostic tests, such as imaging studies or clinical examinations. They are generally safe, non-invasive procedures with few risks or side effects.

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.

The neuromuscular junction (NMJ) is the specialized synapse or chemical communication point, where the motor neuron's nerve terminal (presynaptic element) meets the muscle fiber's motor end plate (postsynaptic element). This junction plays a crucial role in controlling muscle contraction and relaxation.

At the NMJ, the neurotransmitter acetylcholine is released from the presynaptic nerve terminal into the synaptic cleft, following an action potential. Acetylcholine then binds to nicotinic acetylcholine receptors on the postsynaptic membrane of the muscle fiber, leading to the generation of an end-plate potential. If sufficient end-plate potentials are generated and summate, they will trigger an action potential in the muscle fiber, ultimately causing muscle contraction.

Dysfunction at the neuromuscular junction can result in various neuromuscular disorders, such as myasthenia gravis, where autoantibodies attack acetylcholine receptors, leading to muscle weakness and fatigue.

Tandem pore domain potassium (K2P) channels are a subfamily of potassium channels that contain two pore-forming domains in a single polypeptide chain. These channels are also known as "double-barreled" or "leak" potassium channels because they provide a background leak conductance for potassium ions across the cell membrane. They are involved in regulating the resting membrane potential and excitability of cells, and are targets for various therapeutic agents. Examples of K2P channels include TREK, TRAAK, TASK, TWIK, and THIK families.

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.

Pyramidal cells, also known as pyramidal neurons, are a type of multipolar neuron found in the cerebral cortex and hippocampus of the brain. They have a characteristic triangular or pyramid-like shape with a single apical dendrite that extends from the apex of the cell body towards the pial surface, and multiple basal dendrites that branch out from the base of the cell body.

Pyramidal cells are excitatory neurons that play a crucial role in information processing and transmission within the brain. They receive inputs from various sources, including other neurons and sensory receptors, and generate action potentials that are transmitted to other neurons through their axons. The apical dendrite of pyramidal cells receives inputs from distant cortical areas, while the basal dendrites receive inputs from local circuits.

Pyramidal cells are named after their pyramid-like shape and are among the largest neurons in the brain. They are involved in various cognitive functions, including learning, memory, attention, and perception. Dysfunction of pyramidal cells has been implicated in several neurological disorders, such as Alzheimer's disease, epilepsy, and schizophrenia.

Polymyxins are a group of antibiotics derived from the bacterium Paenibacillus polymyxa. They consist of polymyxin B and polymyxin E (also known as colistin), which have similar structures and mechanisms of action. Polymyxins bind to the lipopolysaccharide component of the outer membrane of Gram-negative bacteria, causing disruption of the membrane and ultimately leading to bacterial cell death. These antibiotics are primarily used to treat serious infections caused by multidrug-resistant Gram-negative bacteria, but their use is limited due to potential nephrotoxicity and neurotoxicity.

"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.

The pulmonary artery is a large blood vessel that carries deoxygenated blood from the right ventricle of the heart to the lungs for oxygenation. It divides into two main branches, the right and left pulmonary arteries, which further divide into smaller vessels called arterioles, and then into a vast network of capillaries in the lungs where gas exchange occurs. The thin walls of these capillaries allow oxygen to diffuse into the blood and carbon dioxide to diffuse out, making the blood oxygen-rich before it is pumped back to the left side of the heart through the pulmonary veins. This process is crucial for maintaining proper oxygenation of the body's tissues and organs.

Vasodilator agents are pharmacological substances that cause the relaxation or widening of blood vessels by relaxing the smooth muscle in the vessel walls. This results in an increase in the diameter of the blood vessels, which decreases vascular resistance and ultimately reduces blood pressure. Vasodilators can be further classified based on their site of action:

1. Systemic vasodilators: These agents cause a generalized relaxation of the smooth muscle in the walls of both arteries and veins, resulting in a decrease in peripheral vascular resistance and preload (the volume of blood returning to the heart). Examples include nitroglycerin, hydralazine, and calcium channel blockers.
2. Arterial vasodilators: These agents primarily affect the smooth muscle in arterial vessel walls, leading to a reduction in afterload (the pressure against which the heart pumps blood). Examples include angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and direct vasodilators like sodium nitroprusside.
3. Venous vasodilators: These agents primarily affect the smooth muscle in venous vessel walls, increasing venous capacitance and reducing preload. Examples include nitroglycerin and other organic nitrates.

Vasodilator agents are used to treat various cardiovascular conditions such as hypertension, heart failure, angina, and pulmonary arterial hypertension. It is essential to monitor their use carefully, as excessive vasodilation can lead to orthostatic hypotension, reflex tachycardia, or fluid retention.

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.

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.

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.

Nerve endings, also known as terminal branches or sensory receptors, are the specialized structures present at the termination point of nerve fibers (axons) that transmit electrical signals to and from the central nervous system (CNS). They primarily function in detecting changes in the external environment or internal body conditions and converting them into electrical impulses.

There are several types of nerve endings, including:

1. Free Nerve Endings: These are unencapsulated nerve endings that respond to various stimuli like temperature, pain, and touch. They are widely distributed throughout the body, especially in the skin, mucous membranes, and visceral organs.

2. Encapsulated Nerve Endings: These are wrapped by specialized connective tissue sheaths, which can modify their sensitivity to specific stimuli. Examples include Pacinian corpuscles (responsible for detecting deep pressure and vibration), Meissner's corpuscles (for light touch), Ruffini endings (for stretch and pressure), and Merkel cells (for sustained touch).

3. Specialised Nerve Endings: These are nerve endings that respond to specific stimuli, such as auditory, visual, olfactory, gustatory, and vestibular information. They include hair cells in the inner ear, photoreceptors in the retina, taste buds in the tongue, and olfactory receptors in the nasal cavity.

Nerve endings play a crucial role in relaying sensory information to the CNS for processing and initiating appropriate responses, such as reflex actions or conscious perception of the environment.

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.

The heart ventricles are the two lower chambers of the heart that receive blood from the atria and pump it to the lungs or the rest of the body. The right ventricle pumps deoxygenated blood to the lungs, while the left ventricle pumps oxygenated blood to the rest of the body. Both ventricles have thick, muscular walls to generate the pressure necessary to pump blood through the circulatory system.

FMRFamide is not a medical term per se, but it is a neuropeptide that was first identified in the clam, Mytilus edulis. FMRFamide stands for Phe-Met-Arg-Phe-NH2, which are its five amino acid residues. It functions as a neurotransmitter or neuromodulator in various organisms, including humans. In mammals, related peptides are involved in the regulation of several physiological processes such as cardiovascular function, feeding behavior, and nociception (pain perception).

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.

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."

Vasoconstriction is a medical term that refers to the narrowing of blood vessels due to the contraction of the smooth muscle in their walls. This process decreases the diameter of the lumen (the inner space of the blood vessel) and reduces blood flow through the affected vessels. Vasoconstriction can occur throughout the body, but it is most noticeable in the arterioles and precapillary sphincters, which control the amount of blood that flows into the capillary network.

The autonomic nervous system, specifically the sympathetic division, plays a significant role in regulating vasoconstriction through the release of neurotransmitters like norepinephrine (noradrenaline). Various hormones and chemical mediators, such as angiotensin II, endothelin-1, and serotonin, can also induce vasoconstriction.

Vasoconstriction is a vital physiological response that helps maintain blood pressure and regulate blood flow distribution in the body. However, excessive or prolonged vasoconstriction may contribute to several pathological conditions, including hypertension, stroke, and peripheral vascular diseases.

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.

I believe there might be a misunderstanding in your question. "Dogs" is not a medical term or condition. It is the common name for a domesticated carnivore of the family Canidae, specifically the genus Canis, which includes wolves, foxes, and other extant and extinct species of mammals. Dogs are often kept as pets and companions, and they have been bred in a wide variety of forms and sizes for different purposes, such as hunting, herding, guarding, assisting police and military forces, and providing companionship and emotional support.

If you meant to ask about a specific medical condition or term related to dogs, please provide more context so I can give you an accurate answer.

A seizure is an uncontrolled, abnormal firing of neurons (brain cells) that can cause various symptoms such as convulsions, loss of consciousness, altered awareness, or changes in behavior. Seizures can be caused by a variety of factors including epilepsy, brain injury, infection, toxic substances, or genetic disorders. They can also occur without any identifiable cause, known as idiopathic seizures. Seizures are a medical emergency and require immediate attention.

Ventricular function, in the context of cardiac medicine, refers to the ability of the heart's ventricles (the lower chambers) to fill with blood during the diastole phase and eject blood during the systole phase. The ventricles are primarily responsible for pumping oxygenated blood out to the body (left ventricle) and deoxygenated blood to the lungs (right ventricle).

There are several ways to assess ventricular function, including:

1. Ejection Fraction (EF): This is the most commonly used measure of ventricular function. It represents the percentage of blood that is ejected from the ventricle during each heartbeat. A normal left ventricular ejection fraction is typically between 55% and 70%.
2. Fractional Shortening (FS): This is another measure of ventricular function, which calculates the change in size of the ventricle during contraction as a percentage of the original size. A normal FS for the left ventricle is typically between 25% and 45%.
3. Stroke Volume (SV): This refers to the amount of blood that is pumped out of the ventricle with each heartbeat. SV is calculated by multiplying the ejection fraction by the end-diastolic volume (the amount of blood in the ventricle at the end of diastole).
4. Cardiac Output (CO): This is the total amount of blood that the heart pumps in one minute. It is calculated by multiplying the stroke volume by the heart rate.

Impaired ventricular function can lead to various cardiovascular conditions, such as heart failure, cardiomyopathy, and valvular heart disease. Assessing ventricular function is crucial for diagnosing these conditions, monitoring treatment response, and guiding clinical decision-making.

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.

Sodium is an essential mineral and electrolyte that is necessary for human health. In a medical context, sodium is often discussed in terms of its concentration in the blood, as measured by serum sodium levels. The normal range for serum sodium is typically between 135 and 145 milliequivalents per liter (mEq/L).

Sodium plays a number of important roles in the body, including:

* Regulating fluid balance: Sodium helps to regulate the amount of water in and around your cells, which is important for maintaining normal blood pressure and preventing dehydration.
* Facilitating nerve impulse transmission: Sodium is involved in the generation and transmission of electrical signals in the nervous system, which is necessary for proper muscle function and coordination.
* Assisting with muscle contraction: Sodium helps to regulate muscle contractions by interacting with other minerals such as calcium and potassium.

Low sodium levels (hyponatremia) can cause symptoms such as confusion, seizures, and coma, while high sodium levels (hypernatremia) can lead to symptoms such as weakness, muscle cramps, and seizures. Both conditions require medical treatment to correct.

Neurotransmitter agents are substances that affect the synthesis, storage, release, uptake, degradation, or reuptake of neurotransmitters, which are chemical messengers that transmit signals across a chemical synapse from one neuron to another. These agents can be either agonists, which mimic the action of a neurotransmitter and bind to its receptor, or antagonists, which block the action of a neurotransmitter by binding to its receptor without activating it. They are used in medicine to treat various neurological and psychiatric disorders, such as depression, anxiety, and Parkinson's disease.

Carbenoxolone is a synthetic derivative of glycyrrhizin, which is found in the root of the licorice plant. It has been used in the treatment of gastric and duodenal ulcers due to its ability to increase the mucosal resistance and promote healing. Carbenoxolone works by inhibiting the enzyme 11-beta-hydroxysteroid dehydrogenase, which leads to an increase in the levels of cortisol and other steroids in the body. This can have various effects on the body, including anti-inflammatory and immunosuppressive actions.

However, long-term use of carbenoxolone has been associated with serious side effects such as hypertension, hypokalemia (low potassium levels), and edema (fluid retention). Therefore, its use is generally limited to short-term treatment of gastric and duodenal ulcers.

Medical Definition: Carbenoxolone

A synthetic derivative of glycyrrhizin, used in the treatment of gastric and duodenal ulcers due to its ability to increase mucosal resistance and promote healing. It is an inhibitor of 11-beta-hydroxysteroid dehydrogenase, leading to increased levels of cortisol and other steroids in the body, with potential anti-inflammatory and immunosuppressive effects. However, long-term use is associated with serious side effects such as hypertension, hypokalemia, and edema.

Epilepsy is a chronic neurological disorder characterized by recurrent, unprovoked seizures. These seizures are caused by abnormal electrical activity in the brain, which can result in a wide range of symptoms, including convulsions, loss of consciousness, and altered sensations or behaviors. Epilepsy can have many different causes, including genetic factors, brain injury, infection, or stroke. In some cases, the cause may be unknown.

There are many different types of seizures that can occur in people with epilepsy, and the specific type of seizure will depend on the location and extent of the abnormal electrical activity in the brain. Some people may experience only one type of seizure, while others may have several different types. Seizures can vary in frequency, from a few per year to dozens or even hundreds per day.

Epilepsy is typically diagnosed based on the patient's history of recurrent seizures and the results of an electroencephalogram (EEG), which measures the electrical activity in the brain. Imaging tests such as MRI or CT scans may also be used to help identify any structural abnormalities in the brain that may be contributing to the seizures.

While there is no cure for epilepsy, it can often be effectively managed with medication. In some cases, surgery may be recommended to remove the area of the brain responsible for the seizures. With proper treatment and management, many people with epilepsy are able to lead normal, productive lives.

Excitatory amino acid antagonists are a class of drugs that block the action of excitatory neurotransmitters, particularly glutamate and aspartate, in the brain. These drugs work by binding to and blocking the receptors for these neurotransmitters, thereby reducing their ability to stimulate neurons and produce an excitatory response.

Excitatory amino acid antagonists have been studied for their potential therapeutic benefits in a variety of neurological conditions, including stroke, epilepsy, traumatic brain injury, and neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. However, their use is limited by the fact that blocking excitatory neurotransmission can also have negative effects on cognitive function and memory.

There are several types of excitatory amino acid receptors, including N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainite receptors. Different excitatory amino acid antagonists may target one or more of these receptor subtypes, depending on their specific mechanism of action.

Examples of excitatory amino acid antagonists include ketamine, memantine, and dextromethorphan. These drugs have been used in clinical practice for various indications, such as anesthesia, sedation, and treatment of neurological disorders. However, their use must be carefully monitored due to potential side effects and risks associated with blocking excitatory neurotransmission.

Oxadiazoles are heterocyclic compounds containing a five-membered ring consisting of two carbon atoms, one nitrogen atom, and two oxygen atoms in an alternating sequence. There are three possible isomers of oxadiazole, depending on the position of the nitrogen atom: 1,2,3-oxadiazole, 1,2,4-oxadiazole, and 1,3,4-oxadiazole. These compounds have significant interest in medicinal chemistry due to their diverse biological activities, including anti-inflammatory, antiviral, antibacterial, antifungal, and anticancer properties. Some oxadiazoles also exhibit potential as contrast agents for medical imaging techniques such as magnetic resonance imaging (MRI) and computed tomography (CT).

Bicuculline is a pharmacological agent that acts as a competitive antagonist at GABA-A receptors, which are inhibitory neurotransmitter receptors in the central nervous system. By blocking the action of GABA (gamma-aminobutyric acid) at these receptors, bicuculline can increase neuronal excitability and cause convulsions. It is used in research to study the role of GABAergic neurotransmission in various physiological processes and neurological disorders.

Carbohydrate conformation refers to the three-dimensional shape and structure of a carbohydrate molecule. Carbohydrates, also known as sugars, can exist in various conformational states, which are determined by the rotation of their component bonds and the spatial arrangement of their functional groups.

The conformation of a carbohydrate molecule can have significant implications for its biological activity and recognition by other molecules, such as enzymes or antibodies. Factors that can influence carbohydrate conformation include the presence of intramolecular hydrogen bonds, steric effects, and intermolecular interactions with solvent molecules or other solutes.

In some cases, the conformation of a carbohydrate may be stabilized by the formation of cyclic structures, in which the hydroxyl group at one end of the molecule forms a covalent bond with the carbonyl carbon at the other end, creating a ring structure. The most common cyclic carbohydrates are monosaccharides, such as glucose and fructose, which can exist in various conformational isomers known as anomers.

Understanding the conformation of carbohydrate molecules is important for elucidating their biological functions and developing strategies for targeting them with drugs or other therapeutic agents.

Smooth muscle, also known as involuntary muscle, is a type of muscle that is controlled by the autonomic nervous system and functions without conscious effort. These muscles are found in the walls of hollow organs such as the stomach, intestines, bladder, and blood vessels, as well as in the eyes, skin, and other areas of the body.

Smooth muscle fibers are shorter and narrower than skeletal muscle fibers and do not have striations or sarcomeres, which give skeletal muscle its striped appearance. Smooth muscle is controlled by the autonomic nervous system through the release of neurotransmitters such as acetylcholine and norepinephrine, which bind to receptors on the smooth muscle cells and cause them to contract or relax.

Smooth muscle plays an important role in many physiological processes, including digestion, circulation, respiration, and elimination. It can also contribute to various medical conditions, such as hypertension, gastrointestinal disorders, and genitourinary dysfunction, when it becomes overactive or underactive.

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... may refer to any of several chemical compounds: 2-Aminopyridine 3-Aminopyridine 4-Aminopyridine (4-AP), also ...
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4-membered rings can be obtained by [2+2]cycloadditions for instance with benzyne. An example of a 1,3-dipolar cycloaddition to ... 199 (3-4): 373. Bibcode:1992CPL...199..373C. doi:10.1016/0009-2614(92)80134-W. Ohtsuki, T.; Ohno, K.; Shiga, K.; Kawazoe, Y.; ... C60][ferrocene]2, in which the C60 molecules are arranged in close-packed layers [C60][1,4-dihydroquinone]3 has C60 molecules ... The trimer has also been reported using 4-aminopyridine as catalyst (4% yield) and observed with scanning tunneling microscopy ...
The plan to euthanize the birds drew criticism from wildlife advocates, and the city later stopped the use of 4-Aminopyridine ...
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As a member of the aminopyridine class, besipirdine enhances the release of acetylcholine by blocking M-channels, voltage-gated ... 300 (1-2): 71-4. doi:10.1016/0014-2999(96)00002-7. PMID 8741167. Francis, P. T.; Palmer, A. M.; Snape, M; Wilcock, G. K. (1999 ... Its N-despropyl metabolite, P86-7480, exhibits transient vasoconstrictor effects, producing a pressor effect of 16 ± 4 mm Hg ... Besipirdine (besipirdine hydrochloride, or HP749), an indole-substituted analog of 4-aminopyridine, is a nootropic drug ...
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Solari A, Uitdehaag B, Giuliani G, Pucci E, Taus C (2002). "Aminopyridines for symptomatic treatment in multiple sclerosis". ... Sedehizadeh S, Keogh M, Maddison P (2012). "The use of aminopyridines in neurological disorders". Clinical Neuropharmacology. ... A 2011 Cochrane review compared the cost of the 3,4-DAP and 3,4-DAPP in the UK and found an average price for 3,4-DAP base of £ ... 3,4-Diaminopyridine is a pale yellow to pale brown crystalline powder that melts at about 218-220 °C (424-428 °F) under ...
139 (5 Suppl 4): S47-S81. doi:10.1016/j.otohns.2008.08.022. PMID 18973840. S2CID 16175316. Lay summary in: "ENT doctors release ... 131 (4): 438-444. doi:10.1016/j.otohns.2004.02.046. PMID 15467614. S2CID 28018301. Cohen HS (March 2004). "Side-lying as an ... 2012 (4): CD008675. doi:10.1002/14651858.CD008675.pub2. PMC 6885068. PMID 22513962. Helminski JO, Zee DS, Janssen I, Hain TC ( ... ISBN 978-0-8036-9464-4. Korres SG, Balatsouras DG (October 2004). "Diagnostic, pathophysiologic, and therapeutic aspects of ...
The molecular formula C5H6N2 may refer to: Aminopyridines 2-Aminopyridine 3-Aminopyridine 4-Aminopyridine Diazepines 1,2- ... Diazepine 1,3-Diazepine 1,4-Diazepine Glutaronitrile 1-Vinylimidazole This set index page lists chemical structure articles ...
22 (4): 859-77, vii. doi:10.1016/j.cger.2006.06.011. PMID 17000340. Ilg W, Synofzik M, Brötz D, Burkard S, Giese MA, Schöls L ( ... 19 (4): 605-610. doi:10.1007/s12311-020-01132-8. PMC 7351847. PMID 32328884. Forrest MD, Wall MJ, Press DA, Feng J (December ... 4 (6): 349-361. doi:10.1016/S1474-4422(05)70096-X. PMID 15907739. S2CID 35053543. Moeller JJ, Macaulay RJ, Valdmanis PN, Weston ... 3 (4): 217-227. doi:10.3233/PEP-14097. PMC 4256671. PMID 25485164. Walshe JM. Clarke CE, Nicholl DJ (eds.). "Wilson's Disease ...
... aminopyridines MeSH D03.383.725.050.060 - 4-aminopyridine MeSH D03.383.725.050.085 - amrinone MeSH D03.383.725.050.085.543 - ... 4,5-tetrahydro-8-chloro-3-methyl-5-phenyl-1h-3-benzazepin-7-ol MeSH D03.438.079.800 - 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl ... 4,5-dihydro-1-(3-(trifluoromethyl)phenyl)-1h-pyrazol-3-amine MeSH D03.383.129.539.200 - epirizole MeSH D03.383.129.539.487 - ... 4-oxadiazole MeSH D03.383.312.649.290 - fanft MeSH D03.383.312.649.308 - furagin MeSH D03.383.312.649.313 - furazolidone MeSH ...
4,4'-(3-oxo-1,5-pentanediyl)bis(n,n-dimethyl-n-2-propenyl-), dibromide MeSH D02.092.146.325 - p-dimethylaminoazobenzene MeSH ... 4-nitrophenyl) ester MeSH D02.705.539.783 - phorate MeSH D02.705.539.790 - phosmet MeSH D02.705.539.900 - temefos MeSH D02.705. ... 4-nitrophenyl) ester MeSH D02.886.309.783 - phorate MeSH D02.886.309.790 - phosmet MeSH D02.886.309.900 - temefos MeSH D02.886. ... 4,5-trisphosphate MeSH D02.033.800.519.400.700 - phytic acid MeSH D02.033.800.609 - mannitol MeSH D02.033.800.609.450 - ...
28 (4): 187-91. doi:10.1080/13816810701651233. PMID 18161616. S2CID 46052164. Li N, Wang L, Cui L, Zhang L, Dai S, Li H, et al ... 96 (4): 224-226. doi:10.1016/j.oftal.2020.09.008. PMC 7896820. PMID 33279355. "Beriberi". Genetic and Rare Diseases Information ... Other drugs found to be effective against nystagmus in some patients include memantine, levetiracetam, 3,4-diaminopyridine ( ... 4-aminopyridine, and acetazolamide. Several therapeutic approaches, such as contact lenses, drugs, surgery, and low vision ...
Solari A, Uitdehaag B, Giuliani G, Pucci E, Taus C (2002). Solari A (ed.). "Aminopyridines for symptomatic treatment in ... Wu ZZ, Li DP, Chen SR, Pan HL (December 2009). "Aminopyridines potentiate synaptic and neuromuscular transmission by targeting ... "Aminopyridines potentiate synaptic and neuromuscular transmission by targeting the voltage-activated calcium channel beta ... Aminopyridines, Orphan drugs, Avicides, Multiple Chemboxes, 4-Pyridyl compounds). ...
Potassium Channel4-Aminopyridine(4AP) is a nonselective K+ channel blocker that binds from the cytoplasmic side of the cell ... and aminopyridines in capillary gas-liquid chromatography, Russ. Chem. Bull. (Engl. Transl.), 46(1), 1997, 86-89, In original ... and aminopyridines in capillary gas-liquid chromatography, Russ. Chem. Bull. (Engl. Transl.), 46(1), 1997, 86-89, In original ... p,4-Aminopyridine (4-AP) is a non-selective voltage gated K,sup,+,/sup, channel blocker which blocks K,sub,v,/sub,1.1 and K,sub ...
3-Methyl-4-aminopyridine. Change simulation parameters The result was obtained by a proprietary SIELC algorithm. It may deviate ... 3-Methyl-4-aminopyridine can be analyzed by this reverse phase (RP) HPLC method with simple conditions. The mobile phase ... Separation of 3-Methyl-4-aminopyridine on Newcrom R1 HPLC column. May 17, 2018. ...
Potassium Channel4-Aminopyridine(4AP) is a nonselective K+ channel blocker that binds from the cytoplasmic side of the cell ... and aminopyridines in capillary gas-liquid chromatography, Russ. Chem. Bull. (Engl. Transl.), 46(1), 1997, 86-89, In original ... and aminopyridines in capillary gas-liquid chromatography, Russ. Chem. Bull. (Engl. Transl.), 46(1), 1997, 86-89, In original ... p,4-Aminopyridine (4-AP) is a non-selective voltage gated K,sup,+,/sup, channel blocker which blocks K,sub,v,/sub,1.1 and K,sub ...
ООО "ХИМКРАФТ" / CHEMCRAFT Ltd.. VAT-ID: 3906361820. Reg. number: 1173926029067. Tel: +7 4012 994 890. email: [email protected]. Russia, 236039 Kaliningrad, Bagrationa str. 134/6. ...
Folgering H, Rutten J, Agoston S. Stimulation of Phrenic nerve activity by an acetylcholine releasing drug: 4-aminopyridine. ... Folgering, H., Rutten, J., & Agoston, S. (1979). Stimulation of Phrenic nerve activity by an acetylcholine releasing drug: 4- ... Folgering, H. ; Rutten, J. ; Agoston, S. / Stimulation of Phrenic nerve activity by an acetylcholine releasing drug : 4- ... aminopyridine. In: Pflugers archiv-European journal of physiology. 1979 ; Vol. 379, No. 2. pp. 181-185. ...
4-AMINOPYRIDINE, 504-24-5, Amines & Amine Salts, C5H6N2 by Loba Chemie, India ...
... amino]pyridine. /shop/product/2-amino-3-1-tert-butoxycarbonyl-piperidin-4-yl-amino-pyridine-261655 ¥ 1.00 ¥ 1.00 1.0 CNY ¥ 1.00 ...
Relaxant Effect of 4-Aminopyridine on the Mesenteric Artery of Rat 의 이용 수, 등재여부, 발행기관, 저자, 초록, 목차, 참고문헌 등 논문에 관한 다양한 정보 및 관련논문 ... 4-AP relaxed the sustained contraction induced by 100 mM K,SUP,⁢,/SUP, or Ca,SUP,2⁢,/SUP, ionophore, A23187 (10μM) ... Relaxant Effect of 4-Aminopyridine on the Mesenteric Artery of Rat Relaxant Effect of 4-Aminopyridine on the Mesenteric Artery ... 4-AP (0.1∼10 mM) induced a concentration-dependent relaxation, which was unaffected by NO synthase inhibitor, N,SUP,G,/SUP,- ...
Do not take dalfampridine extended-release tablets together with other aminopyridine medications, including compounded 4-AP ( ... 4 CONTRAINDICATIONS 5 WARNINGS AND PRECAUTIONS 5.1 Seizures 5.2 Renal Impairment 5.3 Concurrent Treatment with Other Forms of 4 ... Aminopyridine 5.4 Anaphylaxis 6 ADVERSE REACTIONS 6.1 Clinical Trials Experience 6.2 Postmarketing Experience 7 DRUG ... When dalfampridine is taken with food, there is a slight increase in Cmax (12 to 17%) and a slight decrease in AUC (4 to 7%). ...
Be sure to mention any other form of 4-aminopyridine (4-AP, fampridine) that has been prepared by your pharmacist. Your doctor ... tell your doctor and pharmacist if you are allergic to dalfampridine, 4-aminopyridine (4-AP, fampridine) that has been prepared ...
4-aminopyridine Treatment for Nerve Injury Resulting From Radical Retro-Pubic Prostatectomy. Lead Researcher: Thomas L Osinski ... To evaluate the role of 4-aminopyridine (4-AP) on the course of recovery after peripheral nerve traction and/or crush injury. ... This study aims to test the hypothesis that 4-aminopyridine speeds the often slow and unpredictable recovery after peripheral ...
Entrapping the 4-AP molecules via hydrogen bond formation.. [54]. Poly (lactic-co-glycolide) Topical vaginal drug delivery. ... Bio Mater. 2021, 4, 3-13. [Google Scholar] [CrossRef]. *Hérou, S.; Bailey, J.J.; Kok, M.; Schlee, P.; Jervis, R.; Brett, D.J.L ... B 2016, 4, 4801-4812. [Google Scholar] [CrossRef][Green Version]. *Rao, S.S.; Nelson, M.T.; Xue, R.; DeJesus, J.K.; Viapiano, M ... The structure of the polymers is presented in Figure 4.. 6.1. Poly(D,L-Lactide-co-Glycolide) (PLGA). PLGA nanofibers made by ...
Han, Y. F., Li, C. P. L., Chow, E., Wang, H., Pang, Y. P., & Carlier, P. R. (1999). Dual-site binding of bivalent 4- ... aminopyridine- and 4-aminoquinoline- based AChE inhibitors: Contribution of the hydrophobic alkylene tether to monomer and ... Han, YF, Li, CPL, Chow, E, Wang, H, Pang, YP & Carlier, PR 1999, Dual-site binding of bivalent 4-aminopyridine- and 4- ... Three series of 4-aminopyridine-and 4-aminoquinoline based symmetrical bivalent acetylcholinesterase (AChE) inhibitors were ...
4-Aminopyridine, A Blocker of Voltage-Dependent K+ Channels, Restores Blood Pressure and Improves Survival in the Wistar Rat ... 4-Aminopyridine, A Blocker of Voltage-Dependent K+ Channels, Restores Blood Pressure and Improves Survival in the Wistar Rat ... 4-Aminopyridine, A Blocker of Voltage-Dependent K+ Channels, Restores Blood Pressure and Improves Survival in the Wistar Rat ... 4-Aminopyridine, A Blocker of Voltage-Dependent K+ Channels, Restores Blood Pressure and Improves Survival in the Wistar Rat ...
4-Aminopyridine: A Single-Dose Diagnostic Agent to Differentiate Axonal Continuity in Nerve Injuries. Military Medicine. 2021 ... Gurjar, A. A., Manto, K. M., Estrada, J. A., Kaufman, M., Sun, D., Talukder, H., & Elfar, J. C. (2021). 4-Aminopyridine: A ... 4-Aminopyridine : A Single-Dose Diagnostic Agent to Differentiate Axonal Continuity in Nerve Injuries. In: Military Medicine. ... 4-Aminopyridine: A Single-Dose Diagnostic Agent to Differentiate Axonal Continuity in Nerve Injuries. / Gurjar, Anagha A.; ...
Pharmacological differences between the two channel types were also found for 4-aminopyridine (4AP). SqKv1As affinity for 4AP ...
Avitrol or 4-Aminopyridine: A bird distress inducing chemical. The affected birds give distress calls that scare other birds ...
2-Amino-pyridine-3-carbaldehyde oximehydrochloride. Catalog Number: 016067 Molecular Formula: C6H8ClN3O ... N-[4-(tert-Butyl-dimethyl-silanyloxymethyl)-pyridin-2-yl]-2,2-dimethyl-propionamide. Catalog Number: 016066 ... 2,2-Dimethyl-N-[3-(4,4,5,5-tetramethyl-[1,3,2]-dioxaborolan-2-yl)-pyridin-2-yl]-propionamide. Catalog Number: 016059 ... N-(4-Hydrazinocarbonyl-pyridin-2-yl)-2,2-dimethyl-propionamide. Catalog Number: 016052 ...
Die Therapie der Wahl bei der Vestibularisparoxysmie ist Carbamazepin (nichtkontrollierte Studie). Aminopyridine, Chlorzoxazone ... Als neues pharmakologisches Therapieprinzip bei zerebell ren Erkrankungen wurden Aminopyridine (Kaliumkanalblocker) zur ... 4. 2013. Anschrift f r die Verfasser. Prof. Dr. med. Michael Strupp, FANA. Neurologische Klinik und Deutsches Zentrum f r. ... 4.. Geser R, Straumann D: Referral and final diagnoses of patients assessed in an academic vertigo center. Front Neurol 2012; 3 ...
4-dimethoxyphenyl)-5-\{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino\}-2-(propan-2-yl)pentanenitrile (ortholog); 4-aminopyridine ... 4. 109,646,024 - 109,647,559 (+). Ensembl. Sscrofa11.1. susScr11. Sscrofa11.1. Sscrofa11.1. 4. 109,646,024 - 109,647,699 (+). ... 4-aminopyridine multiple interactions. ISO. KCNA10 (Homo sapiens). 6480464. 4-Aminopyridine inhibits the reaction [KCNA10 ... 4-Aminopyridine inhibits the reaction [KCNA10 protein results in increased transport of Potassium] more .... CTD. PMID:10836990 ...
Beyond Pesticides, August 12, 2009) A new study examining the effects of the mosquito repellent DEET on insects, mice and human proteins reports that the chemical interferes with a prominent central nervous system enzyme. This effect is magnified when exposure to DEET is combined with exposure to certain other pesticides.. Entitled, "Evidence for inhibition of cholinesterases in insect and mammalian nervous systems by the insect repellent deet," and published in BioMed Central (BMC) Biology, the study utilized toxicological, biochemical and electrophysiological techniques to show that DEET is not simply a behavior-modifying chemical, but that it also inhibits cholinesterase activity in both insect and mammalian neuronal preparations. The researchers examined DEETs effects on mosquitoes, cockroach nerves, mouse muscles, and enzymes purified from fruit flies and humans. Applications of DEET slowed or halted the actions of the enzyme acetylcholinesterase. This enzyme is crucial for regulating ...
Beyond Pesticides, November 5, 2018) As you know, the stakes in this midterm election are high. Many races are too close to call and will be decided by voter turnout. As we have read, our vote will make a difference!. The stakes are high. People and the environment are being poisoned. Pollinators are disappearing. Waterways are being contaminated. Biodiversity is threatened. Children -especially farmworker children-are suffering brain damage, and pesticide exposure is linked to the increase in ADHD and autism. Pesticide exposure is implicated in cancer, Parkinsons disease, reproductive dysfunction, diabetes, learning disabilities, and more.. We need people in elected positions - from local officials to national offices - who will listen to constituents who know the need for protection from pesticides and understand the urgent need to adopt of organic practices. Learn about your candidates and vote!. What more we can do. Take someone with you to the polls. Offer assistance to your neighbors who ...
Baclofen, aminopyridine. Periodic alternating nystagmus. Spontaneous horizontal beating nystagmus, the direction of which ... Table 4. Clinical, Serologic, And Radiologic Features Distinguishing MS, NMOSD, and MOGAD [6, 10, 14, 17, 18, 20, 24, 25] (Open ... Table 4. Clinical, Serologic, And Radiologic Features Distinguishing MS, NMOSD, and MOGAD [6, 10, 14, 17, 18, 20, 24, 25] ... Table 4. Clinical, Serologic, And Radiologic Features Distinguishing MS, NMOSD, and MOGAD [6, 10, 14, 17, 18, 20, 24, 25] ...
Am J Physiol 1995;269(4 pt 1):G606-612.. *. Bolotina VM, Najibi S, Palacino JJ, Pagano PJ, Cohen RA. Nitric oxide directly ... Dig Dis Sci 2001;46(4):822-830.. *. Shi G, Pandolfino JE, Zhang Q, Hirano I, Joehl RJ, Kahrilas PK. Deglutitive inhibition ... These differences include the following: (1) A more depolarized resting membrane potential was found at 4 cm as compared to 2 ... Figure 4: Electrical stimulation of intrinsic nerves in circular smooth muscle strips.. ...
GAA-FGF14 ataxia (SCA27B): phenotypic profile, natural history progression and 4-aminopyridine treatment response. May 11, 2023 ...
There are a few drugs that facilitate acetylcholine release, including tetraethylammonium and 4-aminopyridine. They work by ...
2-Aminopyridine-4-carboxamide *Molecular Formula: C6H7N3O ... 4-(Boc-amino)-2-bromopyridine *Molecular Formula: C10H13BrN2O2 ... 4-Amino-pyridine-3-carboxaldehyde *Molecular Formula: C6H6N2O ... 2-Amino-4-pyridinemethanol *Molecular Formula: C6H8N2O ... 2-Bromopyridine-4-carboxylic acid *Molecular Formula: C6H4BrNO2 ...
2-Aminopyridine. C5H6N2 614 3-Aminopyridine. C5H6N2 615 4-Aminopyridine. C5H6N2 616 Dimethyl propanedinitrile. C5H6N2 ... 4 1 5 H 1.11527891 +1 106.5371264 +1 117.1190329 +1 4 1 13 H 1.09813653 +1 112.2077715 +1 68.1123425 +1 5 4 1 H 1.09957591 +1 ... 4 1 2 C 1.36425269 +1 113.6229724 +1 -131.5849367 +1 1 2 4 N 1.16242086 +1 173.9788593 +1 -113.5229295 +1 6 1 2 H 1.11165416 +1 ...
  • 4-Aminopyridine (4-AP, fampridine, dalfampridine) is an organic compound with the chemical formula C5H4N-NH2. (wikipedia.org)
  • Although improving symptoms, 4-AP does not inhibit progression of MS. Another study, conducted in Brazil, showed that treatment based on fampridine was considered efficient in 70% of the patients. (wikipedia.org)
  • tell your doctor and pharmacist if you are allergic to dalfampridine, 4-aminopyridine (4-AP, fampridine) that has been prepared by your pharmacist, any other medications, or any of the ingredients in dalfampridine tablets. (medlineplus.gov)
  • Be sure to mention any other form of 4-aminopyridine (4-AP, fampridine) that has been prepared by your pharmacist. (medlineplus.gov)
  • AMPYRA should not be taken with other forms of 4-aminopyridine (4-AP, fampridine), since the active ingredient is the same. (ampyra.com)
  • 4-Aminopyridine is also used under the trade name Avitrol as 0.5% or 1% in bird control bait. (wikipedia.org)
  • Avitrol - it contains 4-aminopyridine, which is a central nervous system toxicant. (wildlife-removal.com)
  • There are a few drugs that facilitate acetylcholine release, including tetraethylammonium and 4-aminopyridine. (britannica.com)
  • In calcium entry blocker overdose in humans, 4-aminopyridine can increase the cytosolic Ca2+ concentration very efficiently independent of the calcium channels. (wikipedia.org)
  • 4-AP works as a potassium channel blocker. (wikipedia.org)
  • channel blocker, did not exert any effect on the 4-AP-induced vasorelaxation. (kyobobook.co.kr)
  • Accordingly, treating the stimulated tissue with a potassium channel blocker, 4-aminopyridine, led to the appearance of a shoulder peak in the compound action potential curve. (purdue.edu)
  • An apparent resting state, determined first in the absence of modulators, was recapitulated with the specific inhibitor (1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid and blocker picrotoxin and provided a rationale for bicuculline insensitivity. (bvsalud.org)
  • All allergic 4-aminopyridine-treated rats survived after the induction of anaphylactic shock. (uaeu.ac.ae)
  • Do not take AMPYRA if you have ever had a seizure, have certain types of kidney problems, or are allergic to dalfampridine (4-aminopyridine), the active ingredient in AMPYRA. (ampyra.com)
  • are allergic to dalfampridine (4-aminopyridine), the active ingredient in AMPYRA. (ampyra.com)
  • Conclusions: Our data suggest that voltage-dependent K+ channel inhibition with 4-aminopyridine treatment restores blood pressure and increases survival in the Wistar rat model of anaphylactic shock. (uaeu.ac.ae)
  • Three series of 4-aminopyridine-and 4-aminoquinoline based symmetrical bivalent acetylcholinesterase (AChE) inhibitors were prepared and compared to previously synthesized dimers of 9-amino-1,2,3,4-tetrahydroacridine (tacrine). (elsevierpure.com)
  • Clinical studies have shown that 4-AP is capable of reversing the effects of tetrodotoxin poisoning in animals, however, its effectiveness as an antidote in humans has not yet been determined. (wikipedia.org)
  • 4-Aminopyridine reverses saxitoxin (STX)- and tetrodotoxin (TTX)- induced cardiorespiratory depression in chronically instrumented guinea pigs. (medscape.com)
  • Conclusions: We conclude that 4-AP could be a promising diagnostic agent in differentiating TPNI based on axonal continuity. (elsevierpure.com)
  • 3-Methyl-4-aminopyridine can be analyzed by this reverse phase (RP) HPLC method with simple conditions. (sielc.com)
  • Piridinas sustituidas en cualquier posición con un grupo amino. (bvsalud.org)
  • The objective of this study was to test the ability of 4-aminopyridine to restore blood pressure and increase survival in anaphylactic shock. (uaeu.ac.ae)
  • These results clearly demonstrate that 4-AP can restore nerve conduction and produce muscle response within minutes of administration only when there is a nerve continuity, even in the sedated animal. (elsevierpure.com)
  • However, 4-AP has been shown to potentiate voltage-gated Ca2+ channel currents independent of effects on voltage-activated K+ channels. (wikipedia.org)
  • 4. Yokoyama S, Imoto K, Kawamura T, Higashida H, Iwabe N, Miyata T, and Numa S (1989) Potassium channels from NG108-15 neuroblastoma-glioma hybrid cells: primary structure and functional expression from cDNAs. (aspetjournals.org)
  • 2023-09-18 Buy 4-Dimethylaminopyridine [1122-58-3] ,Linear Formula:C7H10N2 high quality, timely delivery and lower price,Great Customer Support. (chemibd.com)
  • To evaluate the role of 4-aminopyridine (4-AP) on the course of recovery after peripheral nerve traction and/or crush injury. (rochester.edu)
  • In this study, we thought to evaluate the diagnostic potential of 4-AP on the axonal continuity in unawake/sedated animals. (elsevierpure.com)
  • 4-aminopyridine or related voltage-dependent K + channel blockers could be a useful additional therapeutic approach to treatment of refractory anaphylactic shock. (uaeu.ac.ae)
  • Muscle response was measured before crush, after crush, and 30 minutes after systemic 4-AP (150 μg/kg) or local (4-AP)-poly(lactide-co-glycolide)-b-poly(ethylene glycol)-b-poly(lactide-co-glycolide) (PLGA-PEG) treatment. (elsevierpure.com)
  • Single dose of systemic 4-AP and local (4-AP)-PLGA-PEG treatment with crush injury significantly restored muscle responses to electrical stimulation after 30 minutes of administration. (elsevierpure.com)
  • However, systemic 4-AP treatment had no effect on muscle response after nerve transection. (elsevierpure.com)
  • The combined use of microelectrode array technology and 4-aminopyridine-induced chemical stimulation for investigating network-level nociceptive activity in the spinal cord dorsal horn is outlined. (jove.com)
  • Except for amrinone, our results demonstrated antiprotozoal activity for fendiline, mibefradil, and lidoflazine, with IC 50 values in a range between 2 and 16 μ M and Selectivity Index between 4 and 10. (hindawi.com)
  • Spinal cord injury patients have also seen improvement with 4-AP therapy. (wikipedia.org)
  • The MEA 4-AP spinal slice preparation described to you provides a platform to study the connectivity of dorsal horn circuits and how these networks interact during spinal sensory processing. (jove.com)
  • Infectious Mononucleosis Infectious mononucleosis is caused by Epstein-Barr virus (EBV, human herpesvirus type 4) and is characterized by fatigue, fever, pharyngitis, and lymphadenopathy. (msdmanuals.com)
  • Preliminary results in conscious mice suggested a diagnostic role of 4-AP in distinguishing axonal continuity. (elsevierpure.com)
  • Histamine level was higher in controls and the 4-aminopyridine group but reduced in the EPI group. (uaeu.ac.ae)
  • Metabolic acidosis was prevented in the 4-aminopyridine group. (uaeu.ac.ae)
  • This study aims to test the hypothesis that 4-aminopyridine speeds the often slow and unpredictable recovery after peripheral nerve traction and/or crush injuries. (rochester.edu)
  • Although often considered as a single class, CCBs can be subdivided into the following groups depending on chemical structure: dihydropyridines (e.g., nifedipine, nimodipine, and amlodipine), the benzothiazepines (e.g., diltiazem), and phenylalkylamines (e.g., verapamil) [ 4 ]. (hindawi.com)
  • if the dose was sub-lethal, the birds will recover after 4 or more hours without long-term ill effect. (wikipedia.org)
  • A study has shown that 4-AP is a potent calcium channel activator and can improve synaptic and neuromuscular function by directly acting on the calcium channel beta subunit. (wikipedia.org)
  • A long-term study (32 months) indicated that 80-90% of patients who initially responded to 4-AP exhibited long-term benefits. (wikipedia.org)
  • The use of 4-aminopyridine in bird control has been criticized by the Humane Society of the United States. (wikipedia.org)
  • The house or English sparrow is a brown, chunky bird about 5 3/4 inches (15 cm) long, and very common in human-made habitats. (800critter.com)
  • Potassium channel blockers, such as 4-aminopyridine, induce vasoconstriction. (uaeu.ac.ae)
  • Pharmacological differences between the two channel types were also found for 4-aminopyridine (4AP). (nih.gov)
  • 4-aminopyridine (4-AP) is clinically used in multiple sclerosis patients for walking performance improvement. (elsevierpure.com)
  • Case reports have shown that overdoses with 4-AP can lead to paresthesias, seizures, and atrial fibrillation. (wikipedia.org)
  • 4-AP should not be given to people with significant kidney disease (e.g., acute kidney injury or advanced chronic kidney disease) due to the higher risk of seizures with increased circulating levels of 4-AP. (wikipedia.org)
  • envenomation of a 4-year-old boy: a case report. (medscape.com)
  • 4-Aminopyridine is a potent convulsant and is used to generate seizures in animal models for the evaluation of antiseizure agents. (wikipedia.org)