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.
Venoms obtained from Apis mellifera (honey bee) and related species. They contain various enzymes, polypeptide toxins, and other substances, some of which are allergenic or immunogenic or both. These venoms were formerly used in rheumatism to stimulate the pituitary-adrenal system.
A 37-amino acid residue peptide isolated from the scorpion Leiurus quinquestriatus hebraeus. It is a neurotoxin that inhibits calcium activated potassium channels.
A major class of calcium-activated potassium channels that are found primarily in excitable CELLS. They play important roles in the transmission of ACTION POTENTIALS and generate a long-lasting hyperpolarization known as the slow afterhyperpolarization.
Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.
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.
Potassium channels whose activation is dependent on intracellular calcium concentrations.
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.
A potassium-selective ion channel blocker. (From J Gen Phys 1994;104(1):173-90)
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.
That phase of a muscle twitch during which a muscle returns to a resting position.
An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6)
A major class of calcium-activated potassium channels that were originally discovered in ERYTHROCYTES. They are found primarily in non-excitable CELLS and set up electrical gradients for PASSIVE ION TRANSPORT.
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.
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).
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
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.
Arteries which arise from the abdominal aorta and distribute to most of the intestines.
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.
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)
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.
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.
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.
An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.
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)
Drugs used to cause dilation of the blood vessels.
A neuromuscular blocker and active ingredient in CURARE; plant based alkaloid of Menispermaceae.
Paracrine substances produced by the VASCULAR ENDOTHELIUM with VASCULAR SMOOTH MUSCLE relaxation (VASODILATION) activities. Several factors have been identified, including NITRIC OXIDE and PROSTACYCLIN.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
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.
A topical bacteriostat that is available as various salts. It is used in wound dressings and mouth infections and may also have antifungal action, but may cause skin ulceration.
Use of electric potential or currents to elicit biological responses.
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.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
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.
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 non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.
A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.
Inorganic compounds that contain barium as an integral part of the molecule.
The relationship between the dose of an administered drug and the response of the organism to the drug.
The recording of muscular movements. The apparatus is called a myograph, the record or tracing, a myogram. (From Stedman, 25th ed)
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.
Insect members of the superfamily Apoidea, found almost everywhere, particularly on flowers. About 3500 species occur in North America. They differ from most WASPS in that their young are fed honey and pollen rather than animal food.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
A sulfur-containing analog of butyrylcholine which is hydrolyzed by butyrylcholinesterase to butyrate and thiocholine. It is used as a reagent in the determination of butyrylcholinesterase activity.
A sweet viscous liquid food, produced in the honey sacs of various bees from nectar collected from flowers. The nectar is ripened into honey by inversion of its sucrose sugar into fructose and glucose. It is somewhat acidic and has mild antiseptic properties, being sometimes used in the treatment of burns and lacerations.

Acetylcholine-induced membrane potential changes in endothelial cells of rabbit aortic valve. (1/590)

1. Using a microelectrode technique, acetylcholine (ACh)-induced membrane potential changes were characterized using various types of inhibitors of K+ and Cl- channels in rabbit aortic valve endothelial cells (RAVEC). 2. ACh produced transient then sustained membrane hyperpolarizations. Withdrawal of ACh evoked a transient depolarization. 3. High K+ blocked and low K+ potentiated the two ACh-induced hyperpolarizations. Charybdotoxin (ChTX) attenuated the ACh-induced transient and sustained hyperpolarizations; apamin inhibited only the sustained hyperpolarization. In the combined presence of ChTX and apamin, ACh produced a depolarization. 4. In Ca2+-free solution or in the presence of Co2+ or Ni2+, ACh produced a transient hyperpolarization followed by a depolarization. In BAPTA-AM-treated cells, ACh produced only a depolarization. 5. A low concentration of A23187 attenuated the ACh-induced transient, but not the sustained, hyperpolarization. In the presence of cyclopiazonic acid, the hyperpolarization induced by ACh was maintained after ACh removal; this maintained hyperpolarization was blocked by Co2+. 6. Both NPPB and hypertonic solution inhibited the membrane depolarization seen after ACh washout. Bumetanide also attenuated this depolarization. 7. It is concluded that in RAVEC, ACh produces a two-component hyperpolarization followed by a depolarization. It is suggested that ACh-induced Ca2+ release from the storage sites causes a transient hyperpolarization due to activation of ChTX-sensitive K+ channels and that ACh-activated Ca2+ influx causes a sustained hyperpolarization by activating both ChTX- and apamin-sensitive K+ channels. Both volume-sensitive Cl- channels and the Na+-K+-Cl- cotransporter probably contribute to the ACh-induced depolarization.  (+info)

Charybdotoxin and apamin block EDHF in rat mesenteric artery if selectively applied to the endothelium. (2/590)

In rat mesenteric artery, endothelium-derived hyperpolarizing factor (EDHF) is blocked by a combination of apamin and charybdotoxin (ChTX). The site of action of these toxins has not been established. We compared the effects of ChTX and apamin applied selectively to the endothelium and to the smooth muscle. In isometrically mounted arteries, ACh (0.01-10 micrometers), in the presence of indomethacin (2.8 microM) and Nomega-nitro-L-arginine methyl ester (L-NAME) (100 microM), concentration dependently relaxed phenylephrine (PE)-stimulated tone (EC50 50 nM; n = 10). Apamin (50 nM) and ChTX (50 nM) abolished this relaxation (n = 5). In pressurized arteries, ACh (10 microM), applied intraluminally in the presence of indomethacin (2.8 microM) and L-NAME (100 microM), dilated both PE-stimulated (0.3-0.5 microM; n = 5) and myogenic tone (n = 3). Apamin (50 nM ) and ChTX (50 nM) applied intraluminally abolished ACh-induced dilatations. Bath superperfusion of apamin and ChTX did not affect ACh-induced dilatations of either PE-stimulated (n = 5) or myogenic tone (n = 3). This is the first demonstration that ChTX and apamin act selectively on the endothelium to block EDHF-mediated relaxation.  (+info)

Role of K+ channels in A2A adenosine receptor-mediated dilation of the pressurized renal arcuate artery. (3/590)

1. Adenosine A2A receptor-mediated renal vasodilation was investigated by measuring the lumenal diameter of pressurized renal arcuate arteries isolated from the rabbit. 2. The selective A2A receptor agonist CGS21680 dilated the arteries with an EC50 of 130 nM. The CGS21680-induced vasodilation was, on average, 34% less in endothelium-denuded arteries. 3. The maximum response and the EC50 for CGS21680-induced vasodilation in endothelium-intact arteries were not significantly affected by incubation with the K+ channel blockers apamin (100 nM), iberiotoxin (100 nM), 3,4-diaminopyridine (1 mM), glibenclamide (1 microM) or Ba2+ (10 microM). However, a cocktail mixture of these blockers did significantly inhibit the maximum response by almost 40%, and 1 mM Ba2+ alone or 1 mM Ba2+ in addition to the cocktail inhibited the maximum CGS21680-response by 58% and about 75% respectively. 4. CGS21680-induced vasodilation was strongly inhibited when the extracellular K+ level was raised to 20 mM even though the dilator response to 1 microM levcromakalim, a K(ATP) channel opener drug, was unaffected. 5. CGS21680-induced vasodilation was inhibited by 10 microM ouabain, an inhibitor of Na+/K(+)-ATPase, but ouabain had a similar inhibitory effect on vasodilation induced by 30 nM nicardipine (a dihydropyridine Ca2+ antagonist) or 1 microM levcromakalim. 6. The data suggest that K+ channel activation does play a role in A(2A) receptor-mediated renal vasodilation. The inhibitory effect of raised extracellular K+ levels on the A(2A) response may be due to K(+)-induced stimulation of Na+/K(+)-ATPase.  (+info)

Blockade of SK-type Ca2+-activated K+ channels uncovers a Ca2+-dependent slow afterdepolarization in nigral dopamine neurons. (4/590)

Sharp electrode current-clamp recording techniques were used to characterize the response of nigral dopamine (DA)-containing neurons in rat brain slices to injected current pulses applied in the presence of TTX (2 microM) and under conditions in which apamin-sensitive Ca2+-activated K+ channels were blocked. Addition of apamin (100-300 nM) to perfusion solutions containing TTX blocked the pacemaker oscillation in membrane voltage evoked by depolarizing current pulses and revealed an afterdepolarization (ADP) that appeared as a shoulder on the falling phase of the voltage response. ADP were preceded by a ramp-shaped slow depolarization and followed by an apamin-insensitive hyperpolarizing afterpotential (HAP). Although ADPs were observed in all apamin-treated cells, the duration of the response varied considerably between individual neurons and was strongly potentiated by the addition of TEA (2-3 mM). In the presence of TTX, TEA, and apamin, optimal stimulus parameters (0.1 nA, 200-ms duration at -55 to -68 mV) evoked ADP ranging from 80 to 1,020 ms in duration (355.3 +/- 56.5 ms, n = 16). Both the ramp-shaped slow depolarization and the ensuing ADP were markedly voltage dependent but appeared to be mediated by separate conductance mechanisms. Thus, although bath application of nifedipine (10-30 microM) or low Ca2+, high Mg2+ Ringer blocked the ADP without affecting the ramp potential, equimolar substitution of Co2+ for Ca2+ blocked both components of the voltage response. Nominal Ca2+ Ringer containing Co2+ also blocked the HAP evoked between -55 and -68 mV. We conclude that the ADP elicited in DA neurons after blockade of apamin-sensitive Ca2+-activated K+ channels is mediated by a voltage-dependent, L-type Ca2+ channel and represents a transient form of the regenerative plateau oscillation in membrane potential previously shown to underlie apamin-induced bursting activity. These data provide further support for the notion that modulation of apamin-sensitive Ca2+-activated K+ channels in DA neurons exerts a permissive effect on the conductances that are involved in the expression of phasic activity.  (+info)

Differential effects of apamin- and charybdotoxin-sensitive K+ conductances on spontaneous discharge patterns of developing retinal ganglion cells. (5/590)

The spontaneous discharge patterns of developing retinal ganglion cells are thought to play a crucial role in the refinement of early retinofugal projections. To investigate the contributions of intrinsic membrane properties to the spontaneous activity of developing ganglion cells, we assessed the effects of blocking large and small calcium-activated potassium conductances on the temporal pattern of such discharges by means of patch-clamp recordings from the intact retina of developing ferrets. Application of apamin and charybdotoxin (CTX), which selectively block the small and large calcium-activated potassium channels, respectively, resulted in significant changes in spontaneous firings. In cells recorded from the oldest animals [postnatal day 30 (P30)-P45], which manifested relatively sustained discharge patterns, application of either blocker induced bursting activity. With CTX the bursts were highly periodic, short in duration, and of high frequency. In contrast, with apamin the interburst intervals were longer, less regular, and lower in overall spike frequency. These differences between the effects of the two blockers on spontaneous activity were documented by spectral analysis of discharge patterns. Filling cells from which recordings were made with Lucifer yellow revealed that these effects were obtained in all three morphological classes of cells: alpha, beta, and gamma. These findings provide the first evidence that apamin- and CTX-sensitive K+ conductances can have differential effects on the spontaneous discharge patterns of retinal ganglion cells. Remarkably, the bursts of activity obtained after apamin application in more mature neurons appeared very similar to the spontaneous bursting patterns observed in developing neurons. These findings suggest that the maturation of calcium-activated potassium channels, particularly the apamin-sensitive conductance, may contribute to the changes in spontaneous firings exhibited by retinal ganglion cells during the course of normal development.  (+info)

Coordinate regulation of gonadotropin-releasing hormone neuronal firing patterns by cytosolic calcium and store depletion. (6/590)

Elevation of cytosolic free Ca2+ concentration ([Ca2+]i) in excitable cells often acts as a negative feedback signal on firing of action potentials and the associated voltage-gated Ca2+ influx. Increased [Ca2+]i stimulates Ca2+-sensitive K+ channels (IK-Ca), and this, in turn, hyperpolarizes the cell and inhibits Ca2+ influx. However, in some cells expressing IK-Ca the elevation in [Ca2+]i by depletion of intracellular stores facilitates voltage-gated Ca2+ influx. This phenomenon was studied in hypothalamic GT1 neuronal cells during store depletion caused by activation of gonadotropin-releasing hormone (GnRH) receptors and inhibition of endoplasmic reticulum (Ca2+)ATPase with thapsigargin. GnRH induced a rapid spike increase in [Ca2+]i accompanied by transient hyperpolarization, followed by a sustained [Ca2+]i plateau during which the depolarized cells fired with higher frequency. The transient hyperpolarization was caused by the initial spike in [Ca2+]i and was mediated by apamin-sensitive IK-Ca channels, which also were operative during the subsequent depolarization phase. Agonist-induced depolarization and increased firing were independent of [Ca2+]i and were not mediated by inhibition of K+ current, but by facilitation of a voltage-insensitive, Ca2+-conducting inward current. Store depletion by thapsigargin also activated this inward depolarizing current and increased the firing frequency. Thus, the pattern of firing in GT1 neurons is regulated coordinately by apamin-sensitive SK current and store depletion-activated Ca2+ current. This dual control of pacemaker activity facilitates voltage-gated Ca2+ influx at elevated [Ca2+]i levels, but also protects cells from Ca2+ overload. This process may also provide a general mechanism for the integration of voltage-gated Ca2+ influx into receptor-controlled Ca2+ mobilization.  (+info)

Endothelium-derived relaxing, contracting and hyperpolarizing factors of mesenteric arteries of hypertensive and normotensive rats. (7/590)

Differences in the acetylcholine (ACh)-induced endothelium-dependent relaxation and hyperpolarization of the mesenteric arteries of Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were studied. Relaxation was impaired in preparations from SHRSP and tendency to reverse the relaxation was observed at high concentrations of ACh in these preparations. Relaxation was partly blocked by NG-nitro-L-arginine (L-NOARG, 100 microM) and, in the presence of L-NOARG, tendency to reverse the relaxation was observed in response to higher concentrations of ACh, even in preparations from WKY. The relaxation remaining in the presence of L-NOARG was also smaller in preparations from SHRSP. The tendency to reverse the relaxation observed at higher concentrations of ACh in preparations from SHRSP or WKY in the presence of L-NOARG were abolished by indomethacin (10 microM). Elevating the K+ concentration of the incubation medium decreased relaxation in the presence of both indomethacin and L-NOARG. Relaxation in the presence of L-NOARG and indomethacin was reduced by the application of both apamin (5 microM) and charybdotoxin (0.1 microM). This suggests that the relaxation induced by ACh is brought about by both endothelium-derived relaxing factor (EDRF, nitric oxide (NO)) and hyperpolarizing factor (EDHF), which activates Ca2+-sensitive K+ channels. Electrophysiological measurement revealed that ACh induced endothelium-dependent hyperpolarization of the smooth muscle of both preparations in the presence of L-NOARG and indomethacin; the hyperpolarization being smaller in the preparation from SHRSP than that from WKY. These results suggest that the release of both NO and EDHF is reduced in preparations from SHRSP. In addition, indomethacin-sensitive endothelium-derived contracting factor (EDCF) is released from both preparations; the release being increased in preparations from SHRSP.  (+info)

Integrin-regulated secretion of interleukin 4: A novel pathway of mechanotransduction in human articular chondrocytes. (8/590)

Chondrocyte function is regulated partly by mechanical stimulation. Optimal mechanical stimulation maintains articular cartilage integrity, whereas abnormal mechanical stimulation results in development and progression of osteoarthritis (OA). The responses of signal transduction pathways in human articular chondrocytes (HAC) to mechanical stimuli remain unclear. Previous work has shown the involvement of integrins and integrin-associated signaling pathways in activation of plasma membrane apamin-sensitive Ca2+-activated K+ channels that results in membrane hyperpolarization of HAC after 0. 33 Hz cyclical mechanical stimulation. To further investigate mechanotransduction pathways in HAC and show that the hyperpolarization response to mechanical stimulation is a result of an integrin-dependent release of a transferable secreted factor, we used this response. Neutralizing antibodies to interleukin 4 (IL-4) and IL-4 receptor alpha inhibit mechanically induced membrane hyperpolarization and anti-IL-4 antibodies neutralize the hyperpolarizing activity of medium from mechanically stimulated cells. Antibodies to interleukin 1beta (IL-1beta) and cytokine receptors, interleukin 1 receptor type I and the common gamma chain/CD132 (gamma) have no effect on me- chanically induced membrane hyperpolarization. Chondrocytes from IL-4 knockout mice fail to show a membrane hyperpolarization response to cyclical mechanical stimulation. Mechanically induced release of the chondroprotective cytokine IL-4 from HAC with subsequent autocrine/paracrine activity is likely to be an important regulatory pathway in the maintenance of articular cartilage structure and function. Finally, dysfunction of this pathway may be implicated in OA.  (+info)

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.

Bee venom is a poisonous substance that a honeybee (Apis mellifera) injects into the skin of a person or animal when it stings. It's produced in the venom gland and stored in the venom sac of the bee. Bee venom is a complex mixture of proteins, peptides, and other compounds. The main active components of bee venom include melittin, apamin, and phospholipase A2.

Melittin is a toxic peptide that causes pain, redness, and swelling at the site of the sting. It also has hemolytic (red blood cell-destroying) properties. Apamin is a neurotoxin that can affect the nervous system and cause neurological symptoms in severe cases. Phospholipase A2 is an enzyme that can damage cell membranes and contribute to the inflammatory response.

Bee venom has been used in traditional medicine for centuries, particularly in China and other parts of Asia. It's believed to have anti-inflammatory, analgesic (pain-relieving), and immunomodulatory effects. Some studies suggest that bee venom may have therapeutic potential for a variety of medical conditions, including rheumatoid arthritis, multiple sclerosis, and chronic pain. However, more research is needed to confirm these findings and to determine the safety and efficacy of bee venom therapy.

It's important to note that bee stings can cause severe allergic reactions (anaphylaxis) in some people, which can be life-threatening. If you experience symptoms such as difficulty breathing, rapid heartbeat, or hives after being stung by a bee, seek medical attention immediately.

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.

Small-conductance calcium-activated potassium channels (SK channels) are a type of ion channel found in the membranes of excitable cells, such as neurons and muscle cells. They are called "calcium-activated" because their opening is triggered by an increase in intracellular calcium ions (Ca2+), and "potassium channels" because they are selectively permeable to potassium ions (K+).

SK channels have a small conductance, meaning that they allow only a relatively small number of ions to pass through them at any given time. This makes them less influential in shaping the electrical properties of cells compared to other types of potassium channels with larger conductances.

SK channels play important roles in regulating neuronal excitability and neurotransmitter release, as well as controlling the contraction and relaxation of smooth muscle cells. They are activated by calcium ions that enter the cell through voltage-gated calcium channels or other types of Ca2+ channels, and their opening leads to an efflux of K+ ions from the cell. This efflux of positive charges tends to hyperpolarize the membrane potential, making it more difficult for the cell to generate action potentials and release neurotransmitters.

There are three subtypes of SK channels, designated as SK1, SK2, and SK3, which differ in their biophysical properties and sensitivity to pharmacological agents. These channels have been implicated in a variety of physiological processes, including learning and memory, pain perception, blood pressure regulation, and the pathogenesis of certain neurological disorders.

Biological factors are the aspects related to living organisms, including their genes, evolution, physiology, and anatomy. These factors can influence an individual's health status, susceptibility to diseases, and response to treatments. Biological factors can be inherited or acquired during one's lifetime and can interact with environmental factors to shape a person's overall health. Examples of biological factors include genetic predisposition, hormonal imbalances, infections, and chronic medical conditions.

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.

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.

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.

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.

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.

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.

Nitro-L-arginine or Nitroarginine is not a medical term per se, but it is a chemical compound that is sometimes used in medical research and experiments. It is a salt of nitric acid and L-arginine, an amino acid that is important for the functioning of the body.

Nitroarginine is known to inhibit the production of nitric oxide, a molecule that plays a role in various physiological processes such as blood flow regulation, immune response, and neurotransmission. As a result, nitroarginine has been used in research to study the effects of reduced nitric oxide levels on different systems in the body.

It's worth noting that nitroarginine is not approved for use as a medication in humans, and its use is generally limited to laboratory settings.

Intermediate-conductance calcium-activated potassium channels (IKCa) are a type of ion channel found in various cell types, including immune cells, endothelial cells, and neurons. These channels are activated by an increase in intracellular calcium ions (Ca2+) and allow the flow of potassium ions (K+) out of the cell.

IKCa channels have a single-channel conductance that is intermediate between small-conductance (SKCa) and large-conductance (BKCa) calcium-activated potassium channels, typically ranging from 20 to 100 picosiemens (pS). They are encoded by the KCNN4 gene in humans.

The activation of IKCa channels plays a crucial role in regulating various cellular processes, such as membrane potential, calcium signaling, and immune response. For example, in activated immune cells, the opening of IKCa channels helps to repolarize the membrane potential and limit further Ca2+ entry into the cell, thereby modulating cytokine production and inflammatory responses. In endothelial cells, IKCa channel activation can regulate vascular tone and blood flow by controlling the diameter of blood vessels.

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.

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.

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.

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.

The mesenteric arteries are the arteries that supply oxygenated blood to the intestines. There are three main mesenteric arteries: the superior mesenteric artery, which supplies blood to the small intestine (duodenum to two-thirds of the transverse colon) and large intestine (cecum, ascending colon, and the first part of the transverse colon); the inferior mesenteric artery, which supplies blood to the distal third of the transverse colon, descending colon, sigmoid colon, and rectum; and the middle colic artery, which is a branch of the superior mesenteric artery that supplies blood to the transverse colon. These arteries are important in maintaining adequate blood flow to the intestines to support digestion and absorption of nutrients.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Nitric oxide (NO) is a molecule made up of one nitrogen atom and one oxygen atom. In the body, it is a crucial signaling molecule involved in various physiological processes such as vasodilation, immune response, neurotransmission, and inhibition of platelet aggregation. It is produced naturally by the enzyme nitric oxide synthase (NOS) from the amino acid L-arginine. Inhaled nitric oxide is used medically to treat pulmonary hypertension in newborns and adults, as it helps to relax and widen blood vessels, improving oxygenation and blood flow.

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).

Dequalinium is an antimicrobial agent with both antibacterial and antifungal properties. It is commonly used in the form of a salt, such as dequalinium chloride, in various pharmaceutical and medical applications. Dequalinium works by disrupting the bacterial or fungal cell membrane, leading to their death. It is often found in topical creams, ointments, and oral suspensions for treating infections of the skin, mouth, and throat.

The medical definition of 'dequalinium' is:

A quaternary ammonium compound with antimicrobial properties, used as a topical antiseptic and in the treatment of oral candidiasis and other fungal infections. It works by disrupting the bacterial or fungal cell membrane, leading to their death. Dequalinium is available in various forms, including creams, ointments, and oral suspensions.

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

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

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

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

An 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.

The endothelium is a thin layer of simple squamous epithelial cells that lines the interior surface of blood vessels, lymphatic vessels, and heart chambers. The vascular endothelium, specifically, refers to the endothelial cells that line the blood vessels. These cells play a crucial role in maintaining vascular homeostasis by regulating vasomotor tone, coagulation, platelet activation, inflammation, and permeability of the vessel wall. They also contribute to the growth and repair of the vascular system and are involved in various pathological processes such as atherosclerosis, hypertension, and diabetes.

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.

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.

NG-Nitroarginine Methyl Ester (L-NAME) is not a medication, but rather a research chemical used in scientific studies. It is an inhibitor of nitric oxide synthase, an enzyme that synthesizes nitric oxide, a molecule involved in the relaxation of blood vessels.

Therefore, L-NAME is often used in experiments to investigate the role of nitric oxide in various physiological and pathophysiological processes. It is important to note that the use of L-NAME in humans is not approved for therapeutic purposes due to its potential side effects, which can include hypertension, decreased renal function, and decreased cerebral blood flow.

Indomethacin is a non-steroidal anti-inflammatory drug (NSAID) that is commonly used to reduce pain, inflammation, and fever. It works by inhibiting the activity of certain enzymes in the body, including cyclooxygenase (COX), which plays a role in producing prostaglandins, chemicals involved in the inflammatory response.

Indomethacin is available in various forms, such as capsules, suppositories, and injectable solutions, and is used to treat a wide range of conditions, including rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, gout, and bursitis. It may also be used to relieve pain and reduce fever in other conditions, such as dental procedures or after surgery.

Like all NSAIDs, indomethacin can have side effects, including stomach ulcers, bleeding, and kidney damage, especially when taken at high doses or for long periods of time. It may also increase the risk of heart attack and stroke. Therefore, it is important to use indomethacin only as directed by a healthcare provider and to report any unusual symptoms or side effects promptly.

nitroprusside (ni-troe-rus-ide)

A rapid-acting vasodilator used in the management of severe hypertension, acute heart failure, and to reduce afterload in patients undergoing cardiac surgery. It is a potent arterial and venous dilator that decreases preload and afterload, thereby reducing myocardial oxygen demand. Nitroprusside is metabolized to cyanide, which must be monitored closely during therapy to prevent toxicity.

Pharmacologic class: Peripheral vasodilators

Therapeutic class: Antihypertensives, Vasodilators

Medical Categories: Cardiovascular Drugs, Hypertension Agents

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.

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.

I'm sorry for any confusion, but "myography" is not a recognized term in the field of medicine or medical terminology. It may be possible that you have misspelled or misremembered a related term. If you meant "myology," that refers to the study of muscles, their structure, function, and disorders. If you had a different term in mind, please provide it so I can give you a more accurate response.

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.

"Bees" are not a medical term, as they refer to various flying insects belonging to the Apidae family in the Apoidea superfamily. They are known for their role in pollination and honey production. If you're looking for medical definitions or information, please provide relevant terms.

An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.

Butyrylthiocholine is a synthetic chemical compound that is often used in scientific research, particularly in the study of enzymes and neurotransmitters. It is the substrate for the enzyme butyrylcholinesterase, which is found in the blood and helps to break down certain types of drugs and neurotransmitters.

In biochemical terms, butyrylthiocholine is a choline ester of butyric acid, with a thio (sulfur) group replacing one of the oxygen atoms in the ester linkage. This structural feature makes it an excellent substrate for butyrylcholinesterase, as the sulfur atom can form a covalent bond with the enzyme's active site, leading to rapid and specific catalysis.

It is important to note that butyrylthiocholine itself does not have any direct medical relevance, but rather serves as a tool for studying the mechanisms of enzymes and other biological processes.

I'm sorry for any confusion, but "honey" is not typically considered a medical term. It is a natural sweet substance produced by honeybees from the nectar of flowers. Honey is composed primarily of fructose and glucose, with small amounts of other sugars, water, proteins, amino acids, vitamins, minerals, enzymes, and various organic compounds.

While honey does have some potential health benefits, such as its antimicrobial properties and its use in wound healing, it is not a medical treatment or intervention. If you have any questions about the medicinal uses of honey or its role in health, I would recommend consulting with a healthcare professional.

... is an element in bee venom. You can come into contact with apamin through bee venom, so the symptoms that are known are ... Apamin is an 18 amino acid globular peptide neurotoxin found in apitoxin (bee venom). Dry bee venom consists of 2-3% of apamin ... Apamin was first isolated by Habermann in 1965 from Apis mellifera, the Western honey bee. Apamin was named after this bee. Bee ... Apamin is the only neurotoxin acting purely on the central nervous system. The symptoms of apamin toxicity are not well known, ...
Pi4 competes with apamin, another SK-channel toxin. IC50 is 0.5 ± 0.2 μM. Scorpion venoms can be toxic for mammals, insects, ...
Apamin is a neurotoxin that augments polysynaptic reflexes. MCD peptide destroys mast cells. Feeling only slight pain, Schmidt ... Since many small bees are categorized into a pain level of 1, most toxic polypeptides in bee venom are melittin, apamin, and ...
M. Stocker; M. Krause; P. Pedarzani (1999). "An apamin-sentisitive Ca2+-activated K+ current in hippocampal pyramidal neurons ... Examples of calcium-activated potassium channel blockers include: Charybdotoxin Iberiotoxin Apamin Kaliotoxin, Lolitrem, BKCa- ...
Stocker M, Krause M, Pedarzani P (April 1999). "An apamin-sensitive Ca2+-activated K+ current in hippocampal pyramidal neurons ...
Hider RC and Ragnarsson U. A proposal for the structure of apamin. FEBS Letts., 1980; 111, 189-193. Hider RC, Drake AF, Inagaki ...
However, tamapin displaces Apamin in binding assays and is therefore a stronger toxin with respect to Apamin. SK 1 and SK 3 are ... Its sequence similarity to other toxins that can compete with the binding site of apamin is much lower. It is 31 amino acids ... Despite completely different sequences, Apamin (a bee venom toxin) and tamapin share at least in part, the same binding sites ... Tamapin-2 can also compete very effectively with apamin for binding to synaptosomes. The target of tamapin is the small ...
Gmachl, M; Kreil, G (1995). "The precursors of the bee Venom Constituents Apamin and MCD Peptide Are Encoded by two Genes in ... In addition to MCD peptide, melittin and apamin have also been identified in this venom and are also described as voltage- ... Although the MCD peptide sequence shows similarity with apamin, they have different toxic properties. MCD peptide belongs to a ...
In addition, SK channels (SK1-SK3) but not SK4 (IK) are sensitive to blockade by the bee toxin apamin, and the scorpion venoms ... Experiments using apamin have shown that specifically blocking SK channels can increase learning and long-term potentiation. In ... Blatz AL, Magleby KL (1986). "Single apamin-blocked Ca-activated K+ channels of small conductance in cultured rat skeletal ...
Zerrouk; Laraba-Djebari (2009). "Characterization of PO1 a new peptide ligand of the apamin-sensitive Ca2+ activated K+ channel ...
This toxin shows similarity in its physiological activity and binding specificity to apamin, but both toxins show no structural ... potent inhibitor of apamin binding from Leiurus quinquestriatus hebraeus venom". J. Biol. Chem. 263 (21): 10192-7. doi:10.1016/ ...
"Tetraethylammonium blockade of apamin-sensitive and insensitive Ca2+-activated K+ channels in a pituitary cell line." J. ... Inhibition of the electrogenic Na,K pump and Na,K-ATPase activity by tetraethylammonium, tetrabutylammonium, and apamin. ...
Jäger H, Adelman JP, Grissmer S (2000). "SK2 encodes the apamin-sensitive Ca2+-activated K+ channels in the human leukemic T ... 2004). "Calcium-dependent regulation of secretion in biliary epithelial cells: the role of apamin-sensitive SK channels". ...
... which act on apamin-sensitive Ca2+-activated K+ channels". European Journal of Biochemistry. 245 (2): 457-64. doi:10.1111/j. ... injection in mice it could very well compete to binding to the SKCa channel with the toxin iodinated apamin. Kv1.3 channels can ...
"Characterization of a new peptide from Tityus serrulatus scorpion venom which is a ligand of the apamin-binding site". FEBS ...
Unlike other toxins from the same family HsTx1 does not seem to affect the apamin-sensitive calcium-dependent potassium channel ...
It has a high affinity for the 125I-apamin acceptor-binding sites of the rat synaptosomal membranes (Ki = 1.45±0.22 nM) and ... Taicatoxin has an inhibitory effect by reducing the affinity of 125I-apamin for its acceptor and not by alteration of the ... 50 nM of taicatoxin blocks the apamin-sensitive after-hyperpolarizing slow tail K+ currents in rat chromaffin cells, but not ... blocks affinity-labeling of a 33-kDa 125I-apamin-binding polypeptide. Other neurotoxins that act on the calcium channels are ...
... termini and is readily blocked by apamin. The gene for KCa2.3, KCNN3, is located on chromosome 1q21. KCa2.3 is found in the ...
When the stimulus strength was reduced below the action potential threshold, apamin, a neurotoxin, was added to assess the ...
V. crabro venom contains neurotransmitters such as dopamine, serotonin, histamine and noradrenalineneurotoxin apamin, as well ...
On the other hand, TmTx does not seem to inhibit [125I] apamin binding to synaptic membranes in the rat brain or ionomycin- ...
This channel, the apamin sensitive, small conductance SK2 potassium channel, is activated by calcium that is likely released ...
... (MTX) blocks various K+ -channels: Apamin-sensitive small conductance Ca2+ - activated K+ channels (SK) Intermediate ...
Further protein components include apamin (2%), a neurotoxin, hyaluronidase (2%), which dilates blood vessels, increasing their ...
... apamin MeSH D20.888.065.115.580 - melitten MeSH D20.888.065.830 - scorpion venoms MeSH D20.888.065.830.150 - charybdotoxin MeSH ...
... induced relaxation by binding to and thereby opening their apamin-sensitive small conductance (SK) Calcium-activated potassium ...
... apamin MeSH D23.946.833.065.115.580 - melitten MeSH D23.946.833.065.830 - scorpion venoms MeSH D23.946.833.065.830.150 - ...
Apamin is an element in bee venom. You can come into contact with apamin through bee venom, so the symptoms that are known are ... Apamin is an 18 amino acid globular peptide neurotoxin found in apitoxin (bee venom). Dry bee venom consists of 2-3% of apamin ... Apamin was first isolated by Habermann in 1965 from Apis mellifera, the Western honey bee. Apamin was named after this bee. Bee ... Apamin is the only neurotoxin acting purely on the central nervous system. The symptoms of apamin toxicity are not well known, ...
... non-apamin-displacing 4-(aminomethylaryl)pyrazolopyrimidine K(Ca) channel blockers is described and their selectivity against K ... displayed sub-micromolar activity in both a thallium flux and whole-cell electrophysiology assay and did not displace apamin in ... Preliminary SAR studies on non-apamin-displacing 4-(aminomethylaryl)pyrrazolopyrimidine K(Ca) channe…. An exploratory SAR study ... Preliminary SAR studies on non-apamin-displacing 4-(aminomethylaryl)pyrrazolopyrimidine K(Ca) channel blockers. AUTHORS. ...
Apamin, blocker of small conductance Ca2+-activated K+ channels (ab120268) Specific References (11) ...
Categories: Apamin Image Types: Photo, Illustrations, Video, Color, Black&White, PublicDomain, CopyrightRestricted 4 images ...
2013b). Heterogeneous upregulation of apamin-sensitive potassium currents in failing human ventricles. J. Am. Heart Assoc. 32 ( ... Chang, P.-C., Hsieh, Y.-C., Hsueh, C.-H., Weiss, J. N., Lin, S.-F., Chen, P.-S. (2013a). Apamin induces early ... who suggested that KCa2 channel inhibition by the toxin apamin facilitated VF induction (Chan et al., 2015) in rabbits. ... between our study and that of Chan that could explain some of the discrepancies is the use of the pore blocking peptide apamin ...
Bram R, See AP, Amin-Hanjani S. Intervention for symptomatic vertebrobasilar disease. J Neurosurg Sci. 2021 Jan 22. [QxMD ...
... apamin and mastoparan. Toxins 2015, 7, 1126-1150. [Google Scholar] [CrossRef] [PubMed] ...
The main components are peptides: melittin, apamin, peptide 401, adolapin, and protease inhibitors. Bee venom supports the ...
Addition of the small conductance KCa blocker apamin had no effect on ACh-mediated dilation in either control or obese rat ...
Sinopsis: Haruki merupakan seorang siswa SMA pendiam yang kutu buku. Suatu hari dia menemukan jurnal harian milik teman sekelasnya yang ceria, yaitu Yamauchi Sakura, yang ternyata mengidap penyakit pankreas. Haruki pun menghabiskan waktu dengan Sakura sampai Sakura mati. 10 Tahun kemudian, Haruki sudah menjadi guru dan dia mengajar di SMA-nya dulu. Ketika sedang berbicara dengan murid laki-laki yang mirip dengannya, kenangan bersama Sakura mulai terngiang dalam benak. Sementara itu, Kyoko teman baiknya Sakura semasa SMA pun mengenang waktu yang ia habiskan bersama Sakura .... ...
Apamin CAS number: CAS #: 24345-16-2. Product code: APA-001. Source: Bee venom powder ...
Watashi, ni-banme no kanojo de īkara Volume 1
Update setiap hari apa min?. Reply ↓ * Bonbon Desember 10, 2018. Setiap hari apa min? Mimin nyediain nya? ...
In the game, the Nakano quintuplets, protagonist Uesugi Fuutarou, and Fuutarous younger sister Raiha went to the Nakanos private island during the summer break only for three days and two nights. But due a heavy storm, the group is unable to going back and has to spend 2 weeks in the island.. ...
Apdet setiap hari apa min ?. Balas. * doramaindo. berkata: 1 Juni 2018 pukul 9:14 pm ...
Password untuk instal apa min ?. Reply * Admin May 16, 2023 at 7:27 am. · Edit ...
Apamin further prolonged APD80 (pacing cycle length 350 ms) from 187.8±4.3 to 206.9±7.1 (P=.014) in HMR1556-treated, from 209.9 ... Apamin did not further prolong the APD80 in male hearts. The Cai transient duration (CaiTD) was significantly longer in diLQTS ... Apamin did not change CaiTD. CONCLUSION: We conclude that IKAS is abundantly increased in female but not in male ventricles ... Apamin, an IKAS blocker, was then added to determine the magnitude of further QT prolongation. RESULTS: HMR1556, E4031, and ATX ...
Patch lain Yg sesuai sm t99 apa min? Biar work 3 Apr 2020, 17.45.00 ...
Kalau warna ungu muda atasan yang pas warna apa min. Untuk stelan gamis jilbab selutut ada ga warna merah marunungu manggis dan ...
... as we observed decreased sensitivity to apamin. These findings show that damage to the mechanism restraining muscle contraction ...
Ang II challenge replicated such increases in apamin-sensitive SK patch clamp currents as well as in real-time PCR and western ... SK2 current contributions were detected through their sensitivity to apamin block. Ang II treatment increased such SK2 ... SK2 current contributions were detected through their sensitivity to apamin block. Ang II treatment increased such SK2 ... Ang II challenge replicated such increases in apamin-sensitive SK patch clamp currents as well as in real-time PCR and western ...
COOK, N.S. & HOF, R.P. (1988). Cardiovascular effects of apamin and BRL 34915 in rats and rabbits. Br. J. Pharmacol., 93, 121- ...
Ruang lingkup yang terdapat pada ilmu Fikih adalah semua hukum yang berbentuk amaliyah untuk diamalkan oleh setiap mukallaf (Mukallaf artinya orangyang sudah dibebani atau diberi tanggung jawab melaksanakan ajaran syariah Is-lam dengan tanda tanda seperti baligh, berakal, sadar, sudah masuk Islam ...
2003). Role of the cholinergic system and of apamin-sensitive Ca ,sup,2+,/sup,-activated K,sup,+,/sup, channels on rabbit ...
The nitric oxide (NO) mediated dilatation was studied in the presence of charybdotoxin, apamin and indomethacin. ADPbetaS, 2- ... The nitric oxide (NO) mediated dilatation was studied in the presence of charybdotoxin, apamin and indomethacin. ADPbetaS, 2- ... The nitric oxide (NO) mediated dilatation was studied in the presence of charybdotoxin, apamin and indomethacin. ADPbetaS, 2- ... The nitric oxide (NO) mediated dilatation was studied in the presence of charybdotoxin, apamin and indomethacin. ADPbetaS, 2- ...
The current was dependent on Ca(2+) influx but unaffected by apamin and charybdotoxin, two blockers of Ca(2+)-activated K(+) ... The current was dependent on Ca(2+) influx but unaffected by apamin and charybdotoxin, two blockers of Ca(2+)-activated K(+) ...
... apamin def: "An 18 amino acid peptide neurotoxin from bee venom which blocks small-conductance Ca2+-activated K+ channels." [ ... http://en.wikipedia.org/wiki/Apamin "Wikipedia"] synonym: "apamine" EXACT [] synonym: "PubChem_Compound_CID:16129677" RELATED ...
Pentru lapte avem nevoie de 200 gr de migdale inmuiate in apa min 8 ore (cel mai bine este sa lasi migdalele de seara pana ...
... and in occlusion experiments using the SK channel blocker apamin, while apamin wash-in mimics pause reduction. Our findings ... and in occlusion experiments using the SK channel blocker apamin, while apamin wash-in mimics pause reduction. Our findings ...
50 nM apamin, suggesting that endothelium-derived hyperpolarizing factor (EDHF) is the participating dilator. The involvement ... 50 nM apamin, suggesting that endothelium-derived hyperpolarizing factor (EDHF) is the participating dilator. The involvement ...
  • TCs in ex vivo bladders during filling increased dramatically after SCI, and this was related to the loss of regulation provided by SK channels, as we observed decreased sensitivity to apamin. (researchsquare.com)
  • SK2 current contributions were detected through their sensitivity to apamin block. (ox.ac.uk)
  • A sting injects a mixture of chemical compounds including melittin, apamin and others. (duball168.com)
  • Addition of the small conductance K Ca blocker apamin had no effect on ACh-mediated dilation in either control or obese rat vessels, consistent with unaltered SK3 expression. (aspetjournals.org)
  • Apamin is an 18 amino acid globular peptide neurotoxin found in apitoxin (bee venom). (wikipedia.org)
  • The general KCNN/SK/KCa2 channel blocker apamin reverted these effects of CyPPA on microglial proliferation. (cnr.it)
  • Dry bee venom consists of 2-3% of apamin. (wikipedia.org)
  • The first symptoms of apitoxin (bee venom), that are now thought to be caused by apamin, were described back in 1936 by Hahn and Leditschke. (wikipedia.org)
  • Apamin was separated from the other compounds by gel filtration and ion exchange chromatography. (wikipedia.org)
  • Apamin selectively blocks SK channels, a type of Ca2+-activated K+ channel expressed in the central nervous system. (wikipedia.org)
  • Due to its specificity for SK channels, apamin is used as a drug in biomedical research to study the electrical properties of SK channels and their role in the afterhyperpolarizations occurring immediately following an action potential. (wikipedia.org)
  • Binding of apamin to SK channels is mediated by amino acids in the pore region as well as extracellular amino acids of the SK channel. (wikipedia.org)
  • These amino acids are involved in the binding of apamin to the Ca2+-activated K+ channel. (wikipedia.org)
  • Preliminary SAR studies on non-apamin-displacing 4-(aminomethylaryl)pyrrazolopyrimidine K(Ca) channel blockers. (vanderbilt.edu)
  • An exploratory SAR study on a series of potent, non-apamin-displacing 4-(aminomethylaryl)pyrazolopyrimidine K(Ca) channel blockers is described and their selectivity against K(Ca) channel subtypes is reported. (vanderbilt.edu)