A plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of ERECTILE DYSFUNCTION.
Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the actions of endogenous or exogenous adrenergic agonists. Adrenergic alpha-antagonists are used in the treatment of hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma.
Drugs that bind to and block the activation of ADRENERGIC ALPHA-2 RECEPTORS.
One of the two major pharmacological subdivisions of adrenergic receptors that were originally defined by the relative potencies of various adrenergic compounds. The alpha receptors were initially described as excitatory receptors that post-junctionally stimulate SMOOTH MUSCLE contraction. However, further analysis has revealed a more complex picture involving several alpha receptor subtypes and their involvement in feedback regulation.
An imidazoline sympatholytic agent that stimulates ALPHA-2 ADRENERGIC RECEPTORS and central IMIDAZOLINE RECEPTORS. It is commonly used in the management of HYPERTENSION.
A subclass of alpha-adrenergic receptors found on both presynaptic and postsynaptic membranes where they signal through Gi-Go G-PROTEINS. While postsynaptic alpha-2 receptors play a traditional role in mediating the effects of ADRENERGIC AGONISTS, the subset of alpha-2 receptors found on presynaptic membranes signal the feedback inhibition of NEUROTRANSMITTER release.
Drugs that selectively bind to and activate alpha adrenergic receptors.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
A benzodioxane-linked imidazole that has alpha-2 adrenoceptor antagonist activity.
Drugs that bind to but do not activate ADRENERGIC RECEPTORS. Adrenergic antagonists block the actions of the endogenous adrenergic transmitters EPINEPHRINE and NOREPINEPHRINE.
1,4-Diethylene dioxides. Industrial solvents. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), dioxane itself may "reasonably be anticipated to be a carcinogen." (Merck Index, 11th ed)
Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of G-proteins with which they bind; this scheme does not respect the alpha-beta distinction.
A direct acting sympathomimetic used as a vasoconstrictor to relieve nasal congestion. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1251)
Compounds that bind to and activate ADRENERGIC ALPHA-2 RECEPTORS.
An adrenergic alpha-2 agonist used as a sedative, analgesic and centrally acting muscle relaxant in VETERINARY MEDICINE.
A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.
Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS.
A thioxanthine with effects similar to the phenothiazine antipsychotics.
Receptors of CLONIDINE and other IMIDAZOLINES. Activity of the ligands was earlier attributed to ADRENERGIC ALPHA-2 RECEPTORS. Endogenous ligands include AGMATINE, imidazoleacetic acid ribotide, and harman.
The excretory duct of the testes that carries SPERMATOZOA. It rises from the SCROTUM and joins the SEMINAL VESICLES to form the ejaculatory duct.
Decarboxylated arginine, isolated from several plant and animal sources, e.g., pollen, ergot, herring sperm, octopus muscle.
Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals (see ADRENERGIC AGENTS). Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists, see ADRENERGIC ALPHA-AGONISTS) are included here.
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
Dilation of pupils to greater than 6 mm combined with failure of the pupils to constrict when stimulated with light. This condition may occur due to injury of the pupillary fibers in the oculomotor nerve, in acute angle-closure glaucoma, and in ADIE SYNDROME.
Use of electric potential or currents to elicit biological responses.
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.
A mixture of three different hydrogenated derivatives of ERGOTAMINE: DIHYDROERGOCORNINE; DIHYDROERGOCRISTINE; and DIHYDROERGOCRYPTINE. Dihydroergotoxine has been proposed to be a neuroprotective agent and a nootropic agent. The mechanism of its therapeutic actions is not clear, but it can act as an alpha-adrenergic antagonist and a dopamine agonist. The methanesulfonate salts of this mixture of alkaloids are called ERGOLOID MESYLATES.
The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system.
A 9,10alpha-dihydro derivative of ERGOTAMINE. It is used as a vasoconstrictor, specifically for the therapy of MIGRAINE DISORDERS.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A imidazole derivative that is an agonist of ADRENERGIC ALPHA-2 RECEPTORS. It is closely-related to MEDETOMIDINE, which is the racemic form of this compound.
The state of the PENIS when the erectile tissue becomes filled or swollen (tumid) with BLOOD and causes the penis to become rigid and elevated. It is a complex process involving CENTRAL NERVOUS SYSTEM; PERIPHERAL NERVOUS SYSTEMS; HORMONES; SMOOTH MUSCLES; and vascular functions.
An agonist of RECEPTORS, ADRENERGIC ALPHA-2 that is used in veterinary medicine for its analgesic and sedative properties. It is the racemate of DEXMEDETOMIDINE.
The procedure of presenting the conditioned stimulus without REINFORCEMENT to an organism previously conditioned. It refers also to the diminution of a conditioned response resulting from this procedure.
An ergot derivative that is a congener of LYSERGIC ACID DIETHYLAMIDE. It antagonizes the effects of serotonin in blood vessels and gastrointestinal smooth muscle, but has few of the properties of other ergot alkaloids. Methysergide is used prophylactically in migraine and other vascular headaches and to antagonize serotonin in the carcinoid syndrome.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
A group of TETRAHYDRONAPHTHALENES containing a keto oxygen.
An alpha-adrenergic antagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator.
A vasodilator that apparently has direct actions on blood vessels and also increases cardiac output. Tolazoline can interact to some degree with histamine, adrenergic, and cholinergic receptors, but the mechanisms of its therapeutic effects are not clear. It is used in treatment of persistent pulmonary hypertension of the newborn.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
Drugs that bind to and activate adrenergic receptors.
Activities performed to obtain licit or illicit substances.
The synapse between a neuron (presynaptic) and an effector cell other than another neuron (postsynaptic). Neuroeffector junctions include synapses onto muscles and onto secretory cells.
Neurons whose primary neurotransmitter is EPINEPHRINE.
A norepinephrine derivative used as a vasoconstrictor agent.
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 subclass of alpha-adrenergic receptors that mediate contraction of SMOOTH MUSCLE in a variety of tissues such as ARTERIOLES; VEINS; and the UTERUS. They are usually found on postsynaptic membranes and signal through GQ-G11 G-PROTEINS.
An alpha-1 adrenergic agonist that causes prolonged peripheral VASOCONSTRICTION.
A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.
Seven membered heterocyclic rings containing a NITROGEN atom.
A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.
The craniosacral division of the autonomic nervous system. The cell bodies of the parasympathetic preganglionic fibers are in brain stem nuclei and in the sacral spinal cord. They synapse in cranial autonomic ganglia or in terminal ganglia near target organs. The parasympathetic nervous system generally acts to conserve resources and restore homeostasis, often with effects reciprocal to the sympathetic nervous system.
An alpha-2 selective adrenergic agonist used as an antihypertensive agent.
An inhibitor of the enzyme TYROSINE 3-MONOOXYGENASE, and consequently of the synthesis of catecholamines. It is used to control the symptoms of excessive sympathetic stimulation in patients with PHEOCHROMOCYTOMA. (Martindale, The Extra Pharmacopoeia, 30th ed)
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.

Neural modulation of cephalexin intestinal absorption through the di- and tripeptide brush border transporter of rat jejunum in vivo. (1/784)

Intestinal absorption of beta-lactamine antibiotics (e.g., cefixime and cephalexin) has been shown to proceed through the dipeptide carrier system. In a previous study, nifedipine (NFP), an L-type calcium channel blocker, enhanced the absorption of cefixime in vivo but not in vitro, and it was suggested that neural mechanisms might be involved in the effect of NFP. The aim of the present study was to assess the involvement of the nervous system on the intestinal absorption of cephalexin (CFX). To investigate this, we used a single-pass jejunal perfusion technique in rats. NFP and diltiazem enhanced approximately 2-fold the plasma levels of CFX in treated rats versus untreated controls. NFP also increased approximately 2-fold the CFX level in portal plasma and increased urinary excretion of CFX, thus indicating that CFX did effectively increase CFX intestinal absorption. Perfusing high concentrations of dipeptides in the jejunal lumen competitively reduced CFX absorption and inhibited the enhancement of CFX absorption produced by NFP. Hexamethonium and lidocaine inhibited the effect of NFP, whereas atropine, capsaicin, clonidine, and isoproterenol enhanced CFX absorption by the same order of magnitude as NFP. Thus, complex neural networks can modulate the function of the intestinal di- and tripeptide transporter. Sympathetic noradrenergic fibers, intestinal sensory neurons, and nicotinic synapses are involved in the increase of CFX absorption produced by NFP.  (+info)

Facilitatory beta2-adrenoceptors on cholinergic and adrenergic nerve endings of the guinea pig trachea. (2/784)

Using electrical field stimulation of epithelium-denuded intact guinea pig tracheal tube preparations, we studied the presence and role of prejunctional beta2-adrenoceptors by measuring evoked endogenous acetylcholine (ACh) and norepinephrine (NE) release directly. Analysis of ACh and NE was through two HPLC systems with electrochemical detection. Electrical field stimulation (150 mA, 0.8 ms, 16 Hz, 5 min, biphasic pulses) released 29.1 +/- 2.5 pmol ACh/g tissue and 70.2 +/- 6.2 pmol NE/g tissue. Preincubation for 15 min with the selective beta2-adrenoceptor agonist fenoterol (1 microM) increased both ACh and NE overflow to 178 +/- 28 (P < 0.01) and 165 +/- 12% (P < 0.01), respectively, of control values, increases that were abolished completely by the selective beta2-adrenoceptor antagonist ICI-118551 (1 microM). Further experiments with increasing fenoterol concentrations (0.1-100 microM) and different preincubation periods (1, 5, and 15 min) showed a strong and concentration-dependent facilitation of NE release, with maximum response levels decreasing (from nearly 5-fold to only 2.5-fold of control value) with increasing agonist contact time. In contrast, sensitivity of facilitatory beta2-adrenoceptors on cholinergic nerves to fenoterol gradually increased when the incubation period was prolonged; in addition, a bell-shaped concentration-response relationship was found at 15 min of preincubation. Fenoterol concentration-response relationships (15-min agonist preincubation) in the presence of atropine and yohimbine (1 microM each) were similar in the case of NE release, but in the case of ACh release, the bell shape was lost. The results indicate a differential capacity and response time profile of facilitatory prejunctional beta2-adrenoceptors on adrenergic and cholinergic nerve terminals in the guinea pig trachea and suggest that the receptors on adrenergic nerves are more susceptible to desensitization.  (+info)

Effects of clonidine on myocardial beta-adrenergic receptor-adenyl cyclase-cAMP system after scalds in rats. (3/784)

AIM: To study the role of clonidine (Clo) on the myocardial beta-adrenergic receptor (beta-AR)-adenyl cyclase (AC)-cAMP system after the scalds in rats. METHODS: A 30% skin-full-thickness scald was produced by immersing rats in 95 degrees C water for 9 s. Clo 0.1-3.0 mg.kg-1 was injected i.p. to rats at 30 min before scalds, yohimbine (Yoh) 0.05 mg.kg-1 or prazosin (Pra) 0.03 mg.kg-1 to rats at 30 min before i.p. Clo. beta-AR density and affinity, AC activity, phosphoric diester hydrolases (PDH) activity, and cAMP content were determined with radioreceptor assay, indirect method, enzymeradiochemical assay, and radioimmunoassay, respectively. RESULTS: Clo inhibited the decrease of the myocardial beta-AR density, the attenuation of AC activity, and the reduction of cAMP content at 12 h after the scalds. Yoh partially reversed the effects of Clo on the three parameters. But Pra did not. CONCLUSION: Clo reversed the changes of the myocardial beta-AR-AC-cAMP system resulted from the scalds in rats.  (+info)

Differential potentiation of arachidonic acid release by rat alpha2 adrenergic receptor subtypes. (4/784)

CHO transfectants expressing the three subtypes of rat alpha2 adrenergic receptors (alpha2AR): alpha2D, alpha2B, alpha2C were studied to compare the transduction pathways leading to the receptor-mediated stimulation of phospholipase A2 (PLA2) in the corresponding cell lines CHO-2D, CHO-2B, CHO-2C. The alpha2B subtype stimulated the arachidonic acid (AA) release after incubation of the cells with 1 microM epinephrine, whereas alpha2D and alpha2C gave no stimulation. Calcium ionophore A23187 (1 microM) increased the release by a factor of 2-4 in the three strains. When cells were incubated with both epinephrine and Ca2+ ionophore, the AA release differed greatly between cell lines with strong potentiation in CHO-2B (2-3 times greater than Ca2+ ionophore alone), moderate potentiation in CHO-2D, and no potentiation in CHO-2C. The three cell lines each inhibited adenylylcyclase with similar efficiencies when 1 microM epinephrine was used as the agonist. The potentiation depended on both alpha2AR and Gi proteins since yohimbine and pertussis toxin inhibited the process. Pretreatment of CHO-2B cells with MAFP which inhibits both cytosolic and Ca2+-independent PLA2, reduced the release of AA induced by epinephrine+Ca2+ ionophore to basal value, whereas bromoenol lactone, a specific Ca2+-independent PLA2 inhibitor, had no effect. Preincubation of the cells with the intracellular calcium chelator BAPTA gave a dose-dependent inhibition of the arachidonic acid (AA) release. In CHO cells expressing the angiotensin II type 1 receptor, coupled to a Gq protein, the agonist (10-7 M) produced maximal AA release: there was no extra increase when angiotensin and Ca2+ ionophore were added together. There was no increase in the amount of inositol 1,4, 5-triphosphate following stimulation of CHO-2B, -2C, -2D cells with 1 microM epinephrine. Epinephrine led to greater phosphorylation of cPLA2, resulting in an electrophoretic mobility shift for all three cell lines, so inadequate p42/44 MAPKs stimulation was not responsible for the weaker stimulation of cPLA2 in CHO-2C cells. Therefore, the stimulation of cPLA2 by Gi proteins presumably involves another unknown mechanism. The differential stimulation of cPLA2 in these transfectants will be of value to study the actual involvement of the transduction pathways leading to maximal cPLA2 stimulation.  (+info)

Canine external carotid vasoconstriction to methysergide, ergotamine and dihydroergotamine: role of 5-HT1B/1D receptors and alpha2-adrenoceptors. (5/784)

The antimigraine drugs methysergide, ergotamine and dihydroergotamine (DHE) produce selective vasoconstriction in the external carotid bed of vagosympathectomized dogs anaesthetized with pentobarbital and artificially respired, but the receptors involved have not yet been completely characterized. Since the above drugs display affinity for several binding sites, including alpha-adrenoceptors and several 5-HT1 and 5-HT2 receptor subtypes, this study has analysed the mechanisms involved in the above responses. Intracarotid (i.c.) infusions during 1 min of methysergide (31-310 microg min(-1)), ergotamine (0.56-5.6 microg min(-1)) or DHE (5.6-31 microg min(-1)) dose-dependently reduced external carotid blood flow (ECBF) by up to 46+/-4, 37+/-4 and 49+/-5%, respectively. Blood pressure and heart rate remained unchanged. The reductions in ECBF by methysergide were abolished and even reversed to increases in animals pre-treated with GR127935 (10 microg kg(-1), i.v.). The reductions in ECBF by ergotamine and DHE remained unchanged in animals pre-treated (i.v.) with prazosin (300 microg kg(-1)), but were partly antagonized in animals pre-treated with either GR127935 (10 or 30 microg kg(-1)) or yohimbine (1000 microg kg(-1)). Pre-treatment with a combination of GR127935 (30 microg kg(-1)) and yohimbine (1000 microg kg(-1)) abolished the responses to both ergotamine and DHE. The above doses of antagonists were shown to produce selective antagonism at their respective receptors. These results suggest that the external carotid vasoconstrictor responses to methysergide primarily involve 5-HT1B/1D receptors, whereas those to ergotamine and DHE are mediated by 5-HT1B/1D receptors as well as alpha2-adrenoceptors.  (+info)

Effects of vasopressin on the sympathetic contraction of rabbit ear artery during cooling. (6/784)

In order to analyse the effects of arginine-vasopressin on the vascular contraction to sympathetic nerve stimulation during cooling, the isometric response of isolated, 2-mm segments of the rabbit central ear (cutaneous) artery to electrical field stimulation (1-8 Hz) was recorded at 37 and 30 degrees C. Electrical stimulation (37 degrees C) produced frequency-dependent arterial contraction, which was reduced at 30 degrees C and potentiated by vasopressin (10 pM, 100 pM and 1 nM). This potentiation was greater at 30 than at 37 degrees C and was abolished at both temperatures by the antagonist of vasopressin V1 receptors d(CH2)5 Tyr(Me)AVP (100 nM). Desmopressin (1 microM) did not affect the response to electrical stimulation. At 37 degrees C, the vasopressin-induced potentiation was abolished by the purinoceptor antagonist PPADS (30 microM), increased by phentolamine (1 microM) or prazosin (1 microM) and not modified by yohimbine (1 microM), whilst at 30 degrees C, the potentiation was reduced by phentolamine, yohimbine or PPADS, and was not modified by prazosin. The Ca2+-channel blockers, verapamil (10 microM) and NiCl2 (1 mM), abolished the potentiating effects of vasopressin at 37 degrees C whilst verapamil reduced and NiCl2 abolished this potentiation at 30 degrees C. The inhibitor of nitric oxide synthesis, L-NOARG (100 microM), or endothelium removal did not modify the potentiation by vasopressin at 37 and 30 degrees C. Vasopressin also increased the arterial contraction to the alpha2-adrenoceptor agonist BHT-920 (10 microM) and to ATP (2 mM) at 30 and 37 degrees C, but it did not modify the contraction to noradrenaline (1 microM) at either temperature. These results suggest that in cutaneous (ear) arteries, vasopressin potentiaties sympathetic vasoconstriction to a greater extent at 30 than at 37 degrees C by activating vasopressin V1 receptors and Ca2+ channels at both temperatures. At 37 degrees C, the potentiation appears related to activation of the purinoceptor component and, at 30 degrees C, to activation of both purinoceptor and alpha2-adrenoceptor components of the sympathetic response.  (+info)

Recovery of locomotion after ventral and ventrolateral spinal lesions in the cat. II. Effects of noradrenergic and serotoninergic drugs. (7/784)

The effects of serotoninergic and noradrenergic drugs (applied intrathecally) on treadmill locomotion were evaluated in two adult cats subjected to a ventral and ventrolateral spinal lesion (T13). Despite the extensive spinal lesion, severely damaging important descending pathways such as the reticulo- and vestibulospinal tracts, both cats recovered quadrupedal voluntary locomotion. As detailed in a previous paper, the locomotor recovery occurred in three stages defined as early period, when the animal could not walk with its hindlimbs, recovery period, when progressive improvement occurred, and plateau period, when a more stable locomotor performance was observed. At this latter stage, the cats suffered from postural and locomotor deficits, such as poor lateral stability, irregular stepping of the hindlimbs, and inconsistent homolateral fore- and hindlimb coupling. The present study aimed at evaluating the potential of serotoninergic and/or noradrenergic drugs to improve the locomotor abilities in the early and late stages. Both cats were implanted chronically with an intrathecal cannula and electromyographic (EMG) electrodes, which allowed determination, under similar recording conditions, of the locomotor performance pre- and postlesion and comparisons of the effects of different drugs. EMG and kinematic analyses showed that norepinephrine (NE) injected in early and plateau periods improved the regularity of the hindlimb stepping and stabilized the interlimb coupling, permitting to maintain constant locomotion for longer periods of time. Methoxamine, the alpha1-agonist (tested only at the plateau period), had similar effects. In contrast, the alpha2-agonist, clonidine, deteriorated walking. Serotoninergic drugs, such as the neurotransmitter itself, serotonin (5HT), the precursor 5-hydroxytryptophan (5HTP), and the agonist quipazine improved the locomotion by increasing regularity of the hindlimb stepping and by increasing the step cycle duration. In contrast, the 5HT1A agonist 8-hydroxy-dipropylaminotetralin (DPAT) caused foot drag in one of the cats, resulting in frequent stumbling. Injection of combination of methoxamine and quipazine resulted in maintained, regular stepping with smooth movements and good lateral stability. Our results show that the effects of drugs can be integrated to the residual voluntary locomotion and improve some of its postural aspects. However, this work shows clearly that the effects of drugs (such as clonidine) may depend on whether or not the spinal lesion is complete. In a clinical context, this may suggest that different classes of drugs could be used in patients with different types of spinal cord injuries. Possible mechanisms underlying the effect of noradrenergic and serotoninergic drugs on the locomotion after partial spinal lesions are discussed.  (+info)

Effects of A1-adenosine receptor antagonists on purinergic transmission in the guinea-pig vas deferens in vitro. (8/784)

1. Intracellularly recorded excitatory junction potentials (ej.ps) were used to study the effects of adenosine receptor antagonists on neurotransmitter release from postganglionic sympathetic nerve terminals in the guinea-pig vas deferens in vitro. 2. The A1 adenosine receptor antagonists, 8-phenyltheophylline (10 microM) and 8-cyclopentyl-1,3-dipropylxanthine (0.1 microM), increased the amplitude of e.j.ps evoked during trains of 20 stimuli at 1 Hz in the presence, but not in the absence, of the alpha2-adrenoceptor antagonist, yohimbine (1 microM) or the non-selective alpha-adrenoceptor antagonist, phentolamine (1 microM). 3. Adenosine (100 microM) reduced the amplitude of e.j.ps, both in the presence and in the absence of phentolamine (1 microM). This inhibitory effect of adenosine is most likely caused by a reduction in transmitter release as there was no detectable change in spontaneous ej.p. amplitudes. 4. In the presence of phentolamine, application of the adenosine uptake inhibitor, S-(p-nitrobenzyl)-6-thioinosine (0.1 microM), had no effect on ej.p. amplitudes. 5. The phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (100 microM), significantly increased the amplitudes of all e.j.ps evoked during trains of 20 stimuli at 1 Hz, both in the presence and in the absence of phentolamine (1 microM). 6. These results suggest that endogenous adenosine modulates neurotransmitter release by an action at prejunctional A1 adenosine receptors only when alpha2-adrenoceptors are blocked.  (+info)

Yohimbine is defined as an alkaloid derived from the bark of the Pausinystalia yohimbe tree, primarily found in Central Africa. It functions as a selective antagonist of α2-adrenergers, which results in increased noradrenaline levels and subsequent vasodilation, improved sexual dysfunction, and potentially increased energy and alertness.

It is used in traditional medicine for the treatment of erectile dysfunction and as an aphrodisiac, but its efficacy and safety are still subjects of ongoing research and debate. It's important to note that yohimbine can have significant side effects, including anxiety, increased heart rate, and high blood pressure, and should only be used under the supervision of a healthcare professional.

Adrenergic alpha-antagonists, also known as alpha-blockers, are a class of medications that block the effects of adrenaline and noradrenaline at alpha-adrenergic receptors. These receptors are found in various tissues throughout the body, including the smooth muscle of blood vessels, the heart, the genitourinary system, and the eyes.

When alpha-blockers bind to these receptors, they prevent the activation of the sympathetic nervous system, which is responsible for the "fight or flight" response. This results in a relaxation of the smooth muscle, leading to vasodilation (widening of blood vessels), decreased blood pressure, and increased blood flow.

Alpha-blockers are used to treat various medical conditions, such as hypertension (high blood pressure), benign prostatic hyperplasia (enlarged prostate), pheochromocytoma (a rare tumor of the adrenal gland), and certain types of glaucoma.

Examples of alpha-blockers include doxazosin, prazosin, terazosin, and tamsulosin. Side effects of alpha-blockers may include dizziness, lightheadedness, headache, weakness, and orthostatic hypotension (a sudden drop in blood pressure upon standing).

Adrenergic alpha-2 receptor antagonists are a class of medications that block the action of norepinephrine, a neurotransmitter and hormone, at adrenergic alpha-2 receptors. These receptors are found in the central and peripheral nervous system and play a role in regulating various physiological functions such as blood pressure, heart rate, and insulin secretion.

By blocking the action of norepinephrine at these receptors, adrenergic alpha-2 receptor antagonists can increase sympathetic nervous system activity, leading to vasodilation, increased heart rate, and increased insulin secretion. These effects make them useful in the treatment of conditions such as hypotension (low blood pressure), opioid-induced sedation and respiratory depression, and diagnostic procedures that require vasodilation.

Examples of adrenergic alpha-2 receptor antagonists include yohimbine, idazoxan, and atipamezole. It's important to note that these medications can have significant side effects, including hypertension, tachycardia, and agitation, and should be used under the close supervision of a healthcare provider.

Adrenergic receptors are a type of G protein-coupled receptor that bind and respond to catecholamines, such as epinephrine (adrenaline) and norepinephrine (noradrenaline). Alpha adrenergic receptors (α-ARs) are a subtype of adrenergic receptors that are classified into two main categories: α1-ARs and α2-ARs.

The activation of α1-ARs leads to the activation of phospholipase C, which results in an increase in intracellular calcium levels and the activation of various signaling pathways that mediate diverse physiological responses such as vasoconstriction, smooth muscle contraction, and cell proliferation.

On the other hand, α2-ARs are primarily located on presynaptic nerve terminals where they function to inhibit the release of neurotransmitters, including norepinephrine. The activation of α2-ARs also leads to the inhibition of adenylyl cyclase and a decrease in intracellular cAMP levels, which can mediate various physiological responses such as sedation, analgesia, and hypotension.

Overall, α-ARs play important roles in regulating various physiological functions, including cardiovascular function, mood, and cognition, and are also involved in the pathophysiology of several diseases, such as hypertension, heart failure, and neurodegenerative disorders.

Clonidine is an medication that belongs to a class of drugs called centrally acting alpha-agonist hypotensives. It works by stimulating certain receptors in the brain and lowering the heart rate, which results in decreased blood pressure. Clonidine is commonly used to treat hypertension (high blood pressure), but it can also be used for other purposes such as managing withdrawal symptoms from opioids or alcohol, treating attention deficit hyperactivity disorder (ADHD), and preventing migraines. It can be taken orally in the form of tablets or transdermally through a patch applied to the skin. As with any medication, clonidine should be used under the guidance and supervision of a healthcare provider.

**Prazosin** is an antihypertensive drug, which belongs to the class of medications called alpha-blockers. It works by relaxing the muscles in the blood vessels, which helps to lower blood pressure and improve blood flow. Prazosin is primarily used to treat high blood pressure (hypertension), but it may also be used for the management of symptoms related to enlarged prostate (benign prostatic hyperplasia).

In a medical definition context:

Prazosin: A selective α1-adrenergic receptor antagonist, used in the treatment of hypertension and benign prostatic hyperplasia. It acts by blocking the action of norepinephrine on the smooth muscle of blood vessels, resulting in vasodilation and decreased peripheral vascular resistance. This leads to a reduction in blood pressure and an improvement in urinary symptoms associated with an enlarged prostate.

Alpha-2 adrenergic receptors are a type of G protein-coupled receptor that binds catecholamines, such as norepinephrine and epinephrine. These receptors are widely distributed in the central and peripheral nervous system, as well as in various organs and tissues throughout the body.

Activation of alpha-2 adrenergic receptors leads to a variety of physiological responses, including inhibition of neurotransmitter release, vasoconstriction, and reduced heart rate. These receptors play important roles in regulating blood pressure, pain perception, and various cognitive and emotional processes.

There are several subtypes of alpha-2 adrenergic receptors, including alpha-2A, alpha-2B, and alpha-2C, which may have distinct physiological functions and be targeted by different drugs. For example, certain medications used to treat hypertension or opioid withdrawal target alpha-2 adrenergic receptors to produce their therapeutic effects.

Adrenergic alpha-agonists are a type of medication that binds to and activates adrenergic alpha receptors, which are found in the nervous system and other tissues throughout the body. These receptors are activated naturally by chemicals called catecholamines, such as norepinephrine and epinephrine (also known as adrenaline), that are released in response to stress or excitement.

When adrenergic alpha-agonists bind to these receptors, they mimic the effects of catecholamines and cause various physiological responses, such as vasoconstriction (constriction of blood vessels), increased heart rate and force of heart contractions, and relaxation of smooth muscle in the airways.

Adrenergic alpha-agonists are used to treat a variety of medical conditions, including hypertension (high blood pressure), glaucoma, nasal congestion, and attention deficit hyperactivity disorder (ADHD). Examples of adrenergic alpha-agonists include phenylephrine, clonidine, and guanfacine.

It's important to note that adrenergic alpha-agonists can have both beneficial and harmful effects, depending on the specific medication, dosage, and individual patient factors. Therefore, they should only be used under the guidance of a healthcare professional.

Norepinephrine, also known as noradrenaline, is a neurotransmitter and a hormone that is primarily produced in the adrenal glands and is released into the bloodstream in response to stress or physical activity. It plays a crucial role in the "fight-or-flight" response by preparing the body for action through increasing heart rate, blood pressure, respiratory rate, and glucose availability.

As a neurotransmitter, norepinephrine is involved in regulating various functions of the nervous system, including attention, perception, motivation, and arousal. It also plays a role in modulating pain perception and responding to stressful or emotional situations.

In medical settings, norepinephrine is used as a vasopressor medication to treat hypotension (low blood pressure) that can occur during septic shock, anesthesia, or other critical illnesses. It works by constricting blood vessels and increasing heart rate, which helps to improve blood pressure and perfusion of vital organs.

Idazoxan is not a medication that is commonly used in clinical practice, so it may not have a widely accepted "medical definition." However, I can provide some information about what idazoxan is and how it's been studied.

Idazoxan is an investigational drug that belongs to a class of medications called alpha-2 adrenergic receptor antagonists. These drugs work by blocking the action of certain chemicals in the brain called neurotransmitters, which can affect mood, behavior, and various physiological functions.

Idazoxan has been studied for its potential use in treating a variety of conditions, including depression, anxiety, and substance abuse disorders. It has also been investigated as a tool for studying certain aspects of brain function and neurotransmitter systems. However, it has not been approved by regulatory agencies such as the U.S. Food and Drug Administration (FDA) for any specific medical use.

It's worth noting that while idazoxan may have potential therapeutic uses, it is not without risks and side effects. Like many medications, it can interact with other drugs and may cause adverse reactions in some people. As such, it should only be used under the close supervision of a qualified healthcare provider.

Adrenergic antagonists, also known as beta blockers or sympatholytic drugs, are a class of medications that block the effects of adrenaline and noradrenaline (also known as epinephrine and norepinephrine) on the body. These neurotransmitters are part of the sympathetic nervous system and play a role in the "fight or flight" response, increasing heart rate, blood pressure, and respiratory rate.

Adrenergic antagonists work by binding to beta-adrenergic receptors in the body, preventing the neurotransmitters from activating them. This results in a decrease in heart rate, blood pressure, and respiratory rate. These medications are used to treat various conditions such as hypertension, angina, heart failure, arrhythmias, glaucoma, and anxiety disorders.

There are two types of adrenergic antagonists: beta blockers and alpha blockers. Beta blockers selectively bind to beta-adrenergic receptors, while alpha blockers bind to alpha-adrenergic receptors. Some medications, such as labetalol, have both beta and alpha blocking properties.

It is important to note that adrenergic antagonists can interact with other medications and may cause side effects, so it is essential to use them under the guidance of a healthcare professional.

Dioxanes are a group of chemical compounds that contain two oxygen atoms and four carbon atoms, linked together in a cyclic structure. The most common dioxane is called 1,4-dioxane, which is often used as a solvent or as a stabilizer in various industrial and consumer products, such as cosmetics, cleaning agents, and paint strippers.

In the medical field, 1,4-dioxane has been classified as a likely human carcinogen by the U.S. Environmental Protection Agency (EPA) and as a possible human carcinogen by the International Agency for Research on Cancer (IARC). Exposure to high levels of 1,4-dioxane has been linked to an increased risk of cancer in laboratory animals, and there is some evidence to suggest that it may also pose a cancer risk to humans.

It's worth noting that the use of 1,4-dioxane in cosmetics and other personal care products has been controversial, as some studies have found detectable levels of this chemical in these products. However, the levels of exposure from these sources are generally low, and it is unclear whether they pose a significant cancer risk to humans. Nonetheless, some organizations and experts have called for stricter regulations on the use of 1,4-dioxane in consumer products to minimize potential health risks.

Adrenergic receptors are a type of G protein-coupled receptor that bind and respond to catecholamines, which include the neurotransmitters norepinephrine (noradrenaline) and epinephrine (adrenaline). These receptors play a crucial role in the body's "fight or flight" response and are involved in regulating various physiological functions such as heart rate, blood pressure, respiration, and metabolism.

There are nine different subtypes of adrenergic receptors, which are classified into two main groups based on their pharmacological properties: alpha (α) and beta (β) receptors. Alpha receptors are further divided into two subgroups, α1 and α2, while beta receptors are divided into three subgroups, β1, β2, and β3. Each subtype has a unique distribution in the body and mediates distinct physiological responses.

Activation of adrenergic receptors occurs when catecholamines bind to their specific binding sites on the receptor protein. This binding triggers a cascade of intracellular signaling events that ultimately lead to changes in cell function. Different subtypes of adrenergic receptors activate different G proteins and downstream signaling pathways, resulting in diverse physiological responses.

In summary, adrenergic receptors are a class of G protein-coupled receptors that bind catecholamines and mediate various physiological functions. Understanding the function and regulation of these receptors is essential for developing therapeutic strategies to treat a range of medical conditions, including hypertension, heart failure, asthma, and anxiety disorders.

Oxymetazoline is a direct-acting mainly α1-adrenergic receptor agonist, which is primarily used as a nasal decongestant and an ophthalmic vasoconstrictor. It constricts blood vessels, reducing swelling and fluid accumulation in the lining of the nose, thereby providing relief from nasal congestion due to allergies or colds. Oxymetazoline is available over-the-counter in various forms, such as nasal sprays, drops, and creams. It's important to follow the recommended usage guidelines, as prolonged use of oxymetazoline can lead to a rebound effect, causing further congestion.

Adrenergic alpha-2 receptor agonists are a class of medications that bind to and activate adrenergic alpha-2 receptors, which are found in the nervous system and other tissues. These receptors play a role in regulating various bodily functions, including blood pressure, heart rate, and release of certain hormones.

When adrenergic alpha-2 receptor agonists bind to these receptors, they can cause a variety of effects, such as:

* Vasoconstriction (narrowing of blood vessels), which can increase blood pressure
* Decreased heart rate and force of heart contractions
* Suppression of the release of norepinephrine (a hormone and neurotransmitter involved in the "fight or flight" response) from nerve endings
* Analgesia (pain relief)

Adrenergic alpha-2 receptor agonists are used in a variety of medical conditions, including:

* High blood pressure
* Glaucoma (to reduce pressure in the eye)
* Anesthesia (to help prevent excessive bleeding and to provide sedation)
* Opioid withdrawal symptoms (to help manage symptoms such as anxiety, agitation, and muscle aches)

Examples of adrenergic alpha-2 receptor agonists include clonidine, brimonidine, and dexmedetomidine.

Xylazine is a central alpha-2 adrenergic agonist, often used in veterinary medicine as a sedative and analgesic. It can produce profound sedation, muscle relaxation, and analgesia. Xylazine is not approved for use in humans in many countries, including the United States, due to its potential for severe side effects such as respiratory depression, bradycardia (slow heart rate), and hypotension (low blood pressure).

Phentolamine is a non-selective alpha-blocker drug, which means it blocks both alpha-1 and alpha-2 receptors. It works by relaxing the muscle around blood vessels, which increases blood flow and lowers blood pressure. Phentolamine is used medically for various purposes, including the treatment of high blood pressure, the diagnosis and treatment of pheochromocytoma (a tumor that releases hormones causing high blood pressure), and as an antidote to prevent severe hypertension caused by certain medications or substances. It may also be used in diagnostic tests to determine if a patient's blood pressure is reactive to drugs, and it can be used during some surgical procedures to help lower the risk of hypertensive crises.

Phentolamine is available in two forms: an injectable solution and oral tablets. The injectable form is typically administered by healthcare professionals in a clinical setting, while the oral tablets are less commonly used due to their short duration of action and potential for causing severe drops in blood pressure. As with any medication, phentolamine should be taken under the supervision of a healthcare provider, and patients should follow their doctor's instructions carefully to minimize the risk of side effects and ensure the drug's effectiveness.

Adrenergic alpha-1 receptor antagonists, also known as alpha-blockers, are a class of medications that block the effects of the neurotransmitter norepinephrine at alpha-1 receptors. These receptors are found in various tissues throughout the body, including the smooth muscle of blood vessels, the bladder, and the eye.

When norepinephrine binds to alpha-1 receptors, it causes smooth muscle to contract, leading to vasoconstriction (constriction of blood vessels), increased blood pressure, and other effects. By blocking these receptors, alpha-blockers can cause relaxation of smooth muscle, leading to vasodilation (expansion of blood vessels), decreased blood pressure, and other effects.

Alpha-blockers are used in the treatment of various medical conditions, including hypertension (high blood pressure), benign prostatic hyperplasia (enlarged prostate), and pheochromocytoma (a rare tumor of the adrenal gland). Examples of alpha-blockers include doxazosin, prazosin, and terazosin.

It's important to note that while alpha-blockers can be effective in treating certain medical conditions, they can also have side effects, such as dizziness, lightheadedness, and orthostatic hypotension (a sudden drop in blood pressure when standing up). As with any medication, it's important to use alpha-blockers under the guidance of a healthcare provider.

Chlorprothixene is a type of antipsychotic medication that is primarily used to treat chronic schizophrenia and related psychotic disorders. It belongs to a class of drugs known as phenothiazines, which work by blocking dopamine receptors in the brain. This helps to reduce the symptoms of psychosis, such as hallucinations, delusions, and disordered thinking.

Chlorprothixene is available in tablet and injectable forms, and its typical starting dose for adults ranges from 10 to 25 milligrams per day. The dosage may be gradually increased over time based on the individual's response to treatment. Common side effects of chlorprothixene include drowsiness, dizziness, dry mouth, constipation, and weight gain.

It is important to note that chlorprothixene can have serious side effects, including tardive dyskinesia (involuntary muscle movements), neuroleptic malignant syndrome (a rare but potentially fatal reaction to antipsychotic medication), and agranulocytosis (a severe decrease in white blood cell count). As with any medication, chlorprothixene should only be used under the close supervision of a healthcare provider.

Imidazoline receptors are a type of G-protein coupled receptor (GPCR) that are widely distributed throughout the central and peripheral nervous system. They were initially identified through their ability to bind imidazoline compounds, but it is now known that they also bind a variety of other structurally diverse ligands.

There are three subtypes of imidazoline receptors: I1, I2, and I3. The I1 receptor is found in the brain and has been shown to play a role in regulating blood pressure, nociception (pain perception), and neuroprotection. The I2 receptor is also found in the brain and has been implicated in the regulation of dopamine release and the sleep-wake cycle. The I3 receptor is primarily located in the peripheral nervous system and has been shown to play a role in regulating insulin secretion and glucose metabolism.

Imidazoline receptors have attracted interest as potential therapeutic targets for a variety of conditions, including hypertension, pain, neurodegenerative disorders, and metabolic diseases. However, further research is needed to fully understand their functions and therapeutic potential.

The vas deferens is a muscular tube that carries sperm from the epididymis to the urethra during ejaculation in males. It is a part of the male reproductive system and is often targeted in surgical procedures like vasectomy, which is a form of permanent birth control.

Agmatine is a natural decarboxylated derivative of the amino acid L-arginine. It is formed in the body through the enzymatic degradation of arginine by the enzyme arginine decarboxylase. Agmatine is involved in various biological processes, including serving as a neurotransmitter and neuromodulator in the central nervous system. It has been shown to play roles in regulating pain perception, insulin secretion, cardiovascular function, and cell growth. Agmatine can also interact with several receptors, such as imidazoline receptors, α2-adrenergic receptors, and NMDA receptors, which contributes to its diverse physiological effects.

Sympatholytics are a class of drugs that block the action of the sympathetic nervous system, which is the part of the autonomic nervous system responsible for preparing the body for the "fight or flight" response. Sympatholytics achieve this effect by binding to and blocking alpha-adrenergic receptors or beta-adrenergic receptors located in various organs throughout the body, including the heart, blood vessels, lungs, gastrointestinal tract, and urinary system.

Examples of sympatholytic drugs include:

* Alpha blockers (e.g., prazosin, doxazosin)
* Beta blockers (e.g., propranolol, metoprolol)
* Centrally acting sympatholytics (e.g., clonidine, methyldopa)

Sympatholytics are used to treat a variety of medical conditions, including hypertension, angina, heart failure, arrhythmias, and certain neurological disorders. They may also be used to manage symptoms associated with anxiety or withdrawal from alcohol or other substances.

Epinephrine, also known as adrenaline, is a hormone and a neurotransmitter that is produced in the body. It is released by the adrenal glands in response to stress or excitement, and it prepares the body for the "fight or flight" response. Epinephrine works by binding to specific receptors in the body, which causes a variety of physiological effects, including increased heart rate and blood pressure, improved muscle strength and alertness, and narrowing of the blood vessels in the skin and intestines. It is also used as a medication to treat various medical conditions, such as anaphylaxis (a severe allergic reaction), cardiac arrest, and low blood pressure.

Mydriasis is a medical term that refers to the dilation or enlargement of the pupil, which is the black circular opening in the center of the iris (the colored part) of the eye. The pupil normally adjusts its size in response to changes in light levels and emotional state. In mydriasis, the pupil becomes widely dilated and less responsive to light. This can occur naturally due to factors such as strong emotions, fear, or physical exertion, but it can also be caused by certain medications, eye drops, or medical conditions like brain injuries or neurological disorders. It is important to note that mydriasis can affect one or both eyes and may have different clinical significance depending on the context.

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.

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.

Dihydroergotoxine is a semi-synthetic ergot alkaloid, which is derived from the ergot fungus (Claviceps purpurea). It is a mixture of four dihydrogenated ergot alkaloids: dihydroergocristine, dihydroergotamine, dihydroergotoxine, and dihydroalphaergocryptine.

Dihydroergotoxine has been used in the treatment of various medical conditions, including peripheral and cerebral vascular insufficiency, migraine headaches, and orthostatic hypotension. It works by stimulating the release of neurotransmitters such as serotonin, dopamine, and norepinephrine, which help to improve blood flow and reduce symptoms associated with these conditions.

It is important to note that dihydroergotoxine can have serious side effects, including ergotism, a condition characterized by vasoconstriction, muscle cramps, and gangrene. It should be used with caution and under the close supervision of a healthcare provider.

The sympathetic nervous system (SNS) is a part of the autonomic nervous system that operates largely below the level of consciousness, and it functions to produce appropriate physiological responses to perceived danger. It's often associated with the "fight or flight" response. The SNS uses nerve impulses to stimulate target organs, causing them to speed up (e.g., increased heart rate), prepare for action, or otherwise respond to stressful situations.

The sympathetic nervous system is activated due to stressful emotional or physical situations and it prepares the body for immediate actions. It dilates the pupils, increases heart rate and blood pressure, accelerates breathing, and slows down digestion. The primary neurotransmitter involved in this system is norepinephrine (also known as noradrenaline).

Dihydroergotamine is a medication that belongs to a class of drugs called ergot alkaloids. It is a semi-synthetic derivative of ergotamine, which is found naturally in the ergot fungus. Dihydroergotamine is used to treat migraines and cluster headaches.

The drug works by narrowing blood vessels around the brain, which helps to reduce the pain and other symptoms associated with migraines and cluster headaches. It can be administered via injection, nasal spray, or oral tablet. Dihydroergotamine may cause serious side effects, including medication overuse headache, ergotism, and cardiovascular events such as heart attack or stroke. Therefore, it is important to use this medication only as directed by a healthcare provider.

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.

Dexmedetomidine is a medication that belongs to a class of drugs called alpha-2 adrenergic agonists. It is used for sedation and analgesia (pain relief) in critically ill patients, as well as for procedural sedation in adults and children. Dexmedetomidine works by mimicking the effects of natural chemicals in the body that help to regulate sleep, wakefulness, and pain perception.

The medical definition of dexmedetomidine is: "A selective alpha-2 adrenergic agonist used for sedation and analgesia in critically ill patients, as well as for procedural sedation in adults and children. Dexmedetomidine has sedative, anxiolytic, analgesic, and sympatholytic properties, and its effects are mediated by activation of alpha-2 adrenergic receptors in the central nervous system."

It is important to note that dexmedetomidine should only be administered under the close supervision of a healthcare professional, as it can have significant effects on heart rate, blood pressure, and respiratory function.

Penile erection is a physiological response that involves the engagement of the corpus cavernosum and spongiosum (erectile tissue) of the penis with blood, leading to its stiffness and rigidity. This process is primarily regulated by the autonomic nervous system and is influenced by factors such as sexual arousal, emotional state, and certain medications or medical conditions. A penile erection may also occur in non-sexual situations, such as during sleep (nocturnal penile tumescence) or due to other physical stimuli.

Medetomidine is a potent alpha-2 adrenergic agonist used primarily in veterinary medicine as an sedative, analgesic (pain reliever), and sympatholytic (reduces the sympathetic nervous system's activity). It is used for chemical restraint, procedural sedation, and analgesia during surgery or other medical procedures in various animals.

In humans, medetomidine is not approved by the FDA for use but may be used off-label in certain situations, such as sedation during diagnostic procedures. It can cause a decrease in heart rate and blood pressure, so it must be administered carefully and with close monitoring of the patient's vital signs.

Medetomidine is available under various brand names, including Domitor (for veterinary use) and Sedator (for human use in some countries). It can also be found as a combination product with ketamine, such as Dexdomitor/Domitor + Ketamine or Ketamine + Medetomidine.

"Extinction, Psychological" refers to the process by which a conditioned response or behavior becomes weakened and eventually disappears when the behavior is no longer reinforced or rewarded. It is a fundamental concept in learning theory and conditioning.

In classical conditioning, extinction occurs when the conditioned stimulus (CS) is repeatedly presented without the unconditioned stimulus (US), leading to the gradual weakening and eventual disappearance of the conditioned response (CR). For example, if a person learns to associate a tone (CS) with a puff of air to the eye (US), causing blinking (CR), but then the tone is presented several times without the puff of air, the blinking response will become weaker and eventually disappear.

In operant conditioning, extinction occurs when a reinforcer is no longer provided following a behavior, leading to the gradual weakening and eventual disappearance of that behavior. For example, if a child receives candy every time they clean their room (reinforcement), but then the candy is withheld, the child may eventually stop cleaning their room (extinction).

It's important to note that extinction can be a slow process and may require multiple trials or repetitions. Additionally, behaviors that have been extinguished can sometimes reappear in certain circumstances, a phenomenon known as spontaneous recovery.

Methysergide is a medication that belongs to a class of drugs called ergot alkaloids. It is primarily used for the prophylaxis (prevention) of migraine headaches. Methysergide works by narrowing blood vessels around the brain, which is thought to help prevent migraines.

The medical definition of Methysergide is:
A semisynthetic ergot alkaloid derivative used in the prophylaxis of migraine and cluster headaches. It has both agonist and antagonist properties at serotonin receptors, and its therapeutic effects are thought to be related to its ability to block the binding of serotonin to its receptors. However, methysergide can have serious side effects, including fibrotic reactions in various organs, such as the heart, lungs, and kidneys, so it is usually used only for short periods of time and under close medical supervision.

"Inbred strains of rats" are genetically identical rodents that have been produced through many generations of brother-sister mating. This results in a high degree of homozygosity, where the genes at any particular locus in the genome are identical in all members of the strain.

Inbred strains of rats are widely used in biomedical research because they provide a consistent and reproducible genetic background for studying various biological phenomena, including the effects of drugs, environmental factors, and genetic mutations on health and disease. Additionally, inbred strains can be used to create genetically modified models of human diseases by introducing specific mutations into their genomes.

Some commonly used inbred strains of rats include the Wistar Kyoto (WKY), Sprague-Dawley (SD), and Fischer 344 (F344) rat strains. Each strain has its own unique genetic characteristics, making them suitable for different types of research.

A drug interaction is the effect of combining two or more drugs, or a drug and another substance (such as food or alcohol), which can alter the effectiveness or side effects of one or both of the substances. These interactions can be categorized as follows:

1. Pharmacodynamic interactions: These occur when two or more drugs act on the same target organ or receptor, leading to an additive, synergistic, or antagonistic effect. For example, taking a sedative and an antihistamine together can result in increased drowsiness due to their combined depressant effects on the central nervous system.
2. Pharmacokinetic interactions: These occur when one drug affects the absorption, distribution, metabolism, or excretion of another drug. For example, taking certain antibiotics with grapefruit juice can increase the concentration of the antibiotic in the bloodstream, leading to potential toxicity.
3. Food-drug interactions: Some drugs may interact with specific foods, affecting their absorption, metabolism, or excretion. An example is the interaction between warfarin (a blood thinner) and green leafy vegetables, which can increase the risk of bleeding due to enhanced vitamin K absorption from the vegetables.
4. Drug-herb interactions: Some herbal supplements may interact with medications, leading to altered drug levels or increased side effects. For instance, St. John's Wort can decrease the effectiveness of certain antidepressants and oral contraceptives by inducing their metabolism.
5. Drug-alcohol interactions: Alcohol can interact with various medications, causing additive sedative effects, impaired judgment, or increased risk of liver damage. For example, combining alcohol with benzodiazepines or opioids can lead to dangerous levels of sedation and respiratory depression.

It is essential for healthcare providers and patients to be aware of potential drug interactions to minimize adverse effects and optimize treatment outcomes.

Tetralones are not a medical term, but rather a chemical classification. They refer to a class of organic compounds that contain a tetralone ring structure, which is a cyclohexanone fused to a benzene ring. These compounds have various applications in the pharmaceutical industry as intermediates in the synthesis of drugs. Some tetralones have been studied for their potential medicinal properties, such as anti-inflammatory and analgesic effects, but they are not themselves approved medical treatments.

Phenoxybenzamine is an antihypertensive medication that belongs to a class of drugs known as non-selective alpha blockers. It works by blocking both alpha-1 and alpha-2 receptors, which results in the relaxation of smooth muscle tissue in blood vessel walls and other organs. This leads to a decrease in peripheral vascular resistance and a reduction in blood pressure.

Phenoxybenzamine is primarily used for the preoperative management of patients with pheochromocytoma, a rare tumor that produces excessive amounts of catecholamines, such as adrenaline and noradrenaline. By blocking alpha receptors, phenoxybenzamine prevents the hypertensive crisis that can occur during surgery to remove the tumor.

It's important to note that phenoxybenzamine has a long duration of action (up to 14 days) and can cause orthostatic hypotension, tachycardia, and other side effects. Therefore, it should be used with caution and under the close supervision of a healthcare professional.

Tolazoline is a medication that acts as an alpha-adrenergic antagonist and a weak peripheral vasodilator. It is primarily used in the treatment of digital ischemia, which is a lack of blood flow to the fingers or toes, often caused by diseases such as scleroderma or Raynaud's phenomenon. Tolazoline works by relaxing the blood vessels and improving blood flow to the affected areas.

It is important to note that the use of tolazoline is limited due to its potential for causing serious side effects, including hypotension (low blood pressure), tachycardia (rapid heart rate), and cardiac arrhythmias (irregular heart rhythms). Therefore, it should only be used under the close supervision of a healthcare provider.

Phenylephrine is a medication that belongs to the class of drugs known as sympathomimetic amines. It primarily acts as an alpha-1 adrenergic receptor agonist, which means it stimulates these receptors, leading to vasoconstriction (constriction of blood vessels). This effect can be useful in various medical situations, such as:

1. Nasal decongestion: When applied topically in the nose, phenylephrine causes constriction of the blood vessels in the nasal passages, which helps to relieve congestion and swelling. It is often found in over-the-counter (OTC) cold and allergy products.
2. Ocular circulation: In ophthalmology, phenylephrine is used to dilate the pupils before eye examinations. The increased pressure from vasoconstriction helps to open up the pupil, allowing for a better view of the internal structures of the eye.
3. Hypotension management: In some cases, phenylephrine may be given intravenously to treat low blood pressure (hypotension) during medical procedures like spinal anesthesia or septic shock. The vasoconstriction helps to increase blood pressure and improve perfusion of vital organs.

It is essential to use phenylephrine as directed, as improper usage can lead to adverse effects such as increased heart rate, hypertension, arrhythmias, and rebound congestion (when used as a nasal decongestant). Always consult with a healthcare professional for appropriate guidance on using this medication.

Adrenergic agonists are medications or substances that bind to and activate adrenergic receptors, which are a type of receptor in the body that respond to neurotransmitters such as norepinephrine and epinephrine (also known as adrenaline).

There are two main types of adrenergic receptors: alpha and beta receptors. Alpha-adrenergic agonists activate alpha receptors, while beta-adrenergic agonists activate beta receptors. These medications can have a variety of effects on the body, depending on which type of receptor they act on.

Alpha-adrenergic agonists are often used to treat conditions such as nasal congestion, glaucoma, and low blood pressure. Examples include phenylephrine, oxymetazoline, and clonidine.

Beta-adrenergic agonists are commonly used to treat respiratory conditions such as asthma and COPD (chronic obstructive pulmonary disease). They work by relaxing the smooth muscle in the airways, which makes it easier to breathe. Examples include albuterol, salmeterol, and formoterol.

It's important to note that adrenergic agonists can have both desired and undesired effects on the body. They should be used under the guidance of a healthcare professional, who can monitor their effectiveness and potential side effects.

Drug-seeking behavior is a term used in the medical field to describe a pattern of actions taken by a person who is trying to obtain drugs, typically prescription medications, for non-medical reasons or in a manner that is considered inappropriate or abusive. This can include behaviors such as:

* Exaggerating symptoms or faking illness to obtain drugs
* Visiting multiple doctors or pharmacies to obtain multiple prescriptions (a practice known as "doctor shopping")
* Using false names or identities to obtain drugs
* Stealing, forging, or altering prescriptions
* Offering to sell or trade prescription medications

Drug-seeking behavior can be a sign of a substance use disorder, such as addiction, and may require medical intervention and treatment. It is important for healthcare providers to be aware of the signs of drug-seeking behavior and to take appropriate measures to ensure that patients are receiving the care and treatment they need while also protecting the integrity of the healthcare system.

A neuroeffector junction is the site where a neuron communicates with an effector cell, such as a muscle fiber or gland. This communication typically occurs through the release of neurotransmitters from the neuron's terminal button, which then bind to receptors on the effector cell and trigger a response. The neuroeffector junction is also sometimes referred to as a synapse or a neuromuscular junction (when it involves a muscle fiber).

Adrenergic neurons are specialized type of nerve cells that release and utilize catecholamines, particularly norepinephrine (noradrenaline) and to a lesser extent, epinephrine (adrenaline), as their primary neurotransmitters. These neurotransmitters play crucial roles in the body's sympathetic nervous system, which is responsible for the "fight or flight" response during stressful situations.

Adrenergic neurons are primarily located in the central nervous system (CNS) and the peripheral nervous system (PNS). In the CNS, they are found mainly in brainstem nuclei, such as the locus coeruleus, which is the primary source of norepinephrine. In the PNS, adrenergic neurons are part of the sympathetic ganglia and innervate various target organs, including the heart, blood vessels, lungs, glands, and other smooth muscles.

The activation of adrenergic receptors by norepinephrine or epinephrine leads to a range of physiological responses, such as increased heart rate, contractility, and blood pressure; bronchodilation in the lungs; and modulation of pain perception, attention, and arousal in the CNS. Dysfunction of adrenergic neurons has been implicated in several neurological and psychiatric disorders, including depression, anxiety, post-traumatic stress disorder (PTSD), and neurodegenerative diseases like Parkinson's disease.

Nordefrin is not typically used as a medical diagnosis or treatment, but it is a medication that contains the active ingredient Noradrenaline (also known as Norepinephrine) which is a naturally occurring hormone and neurotransmitter in the human body.

Noradrenaline is a potent vasoconstrictor, increasing blood pressure and improving blood flow to vital organs such as the heart and brain. It also acts as a bronchodilator, opening up the airways in the lungs. Nordefrin is used as a medication to treat hypotension (low blood pressure) and shock, particularly in cases where other treatments have been ineffective.

It's important to note that Nordefrin should only be administered under the supervision of a healthcare professional, as it can have serious side effects if not used correctly.

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.

Alpha-1 adrenergic receptors (also known as α1-adrenoreceptors) are a type of G protein-coupled receptor that binds catecholamines, such as norepinephrine and epinephrine. These receptors are primarily found in the smooth muscle of various organs, including the vasculature, heart, liver, kidneys, gastrointestinal tract, and genitourinary system.

When an alpha-1 adrenergic receptor is activated by a catecholamine, it triggers a signaling cascade that leads to the activation of phospholipase C, which in turn activates protein kinase C and increases intracellular calcium levels. This ultimately results in smooth muscle contraction, increased heart rate and force of contraction, and vasoconstriction.

Alpha-1 adrenergic receptors are also found in the central nervous system, where they play a role in regulating wakefulness, attention, and anxiety. There are three subtypes of alpha-1 adrenergic receptors (α1A, α1B, and α1D), each with distinct physiological roles and pharmacological properties.

In summary, alpha-1 adrenergic receptors are a type of G protein-coupled receptor that binds catecholamines and mediates various physiological responses, including smooth muscle contraction, increased heart rate and force of contraction, vasoconstriction, and regulation of wakefulness and anxiety.

Methoxamine is a synthetic, selective α1-adrenergic receptor agonist used in scientific research and for therapeutic purposes. It has the ability to stimulate the α1 adrenergic receptors, leading to vasoconstriction (constriction of blood vessels), increased blood pressure, and reduced blood flow to the skin and extremities.

In a medical context, methoxamine is primarily used as an experimental drug or in research settings due to its specific pharmacological properties. It may be employed to investigate the role of α1-adrenergic receptors in various physiological processes or to temporarily counteract the hypotensive (low blood pressure) effects of certain medications, such as vasodilators or anesthetics.

It is important to note that methoxamine is not commonly used in routine clinical practice due to its strong vasoconstrictive properties and potential adverse effects on organ function if misused or improperly dosed.

Catecholamines are a group of hormones and neurotransmitters that are derived from the amino acid tyrosine. The most well-known catecholamines are dopamine, norepinephrine (also known as noradrenaline), and epinephrine (also known as adrenaline). These hormones are produced by the adrenal glands and are released into the bloodstream in response to stress. They play important roles in the "fight or flight" response, increasing heart rate, blood pressure, and alertness. In addition to their role as hormones, catecholamines also function as neurotransmitters, transmitting signals in the nervous system. Disorders of catecholamine regulation can lead to a variety of medical conditions, including hypertension, mood disorders, and neurological disorders.

Azepines are heterocyclic chemical compounds that contain a seven-membered ring with one nitrogen atom and six carbon atoms. The term "azepine" refers to the basic structure, and various substituted azepines exist with different functional groups attached to the carbon and nitrogen atoms.

Azepines are not typically used in medical contexts as a therapeutic agent or a target for drug design. However, some azepine derivatives have been investigated for their potential biological activities, such as anti-inflammatory, antiviral, and anticancer properties. These compounds may be the subject of ongoing research, but they are not yet established as medical treatments.

It's worth noting that while azepines themselves are not a medical term, some of their derivatives or analogs may have medical relevance. Therefore, it is essential to consult medical literature and databases for accurate and up-to-date information on the medical use of specific azepine compounds.

Propranolol is a medication that belongs to a class of drugs called beta blockers. Medically, it is defined as a non-selective beta blocker, which means it blocks the effects of both epinephrine (adrenaline) and norepinephrine (noradrenaline) on the heart and other organs. These effects include reducing heart rate, contractility, and conduction velocity, leading to decreased oxygen demand by the myocardium. Propranolol is used in the management of various conditions such as hypertension, angina pectoris, arrhythmias, essential tremor, anxiety disorders, and infants with congenital heart defects. It may also be used to prevent migraines and reduce the risk of future heart attacks. As with any medication, it should be taken under the supervision of a healthcare provider due to potential side effects and contraindications.

The Parasympathetic Nervous System (PNS) is the part of the autonomic nervous system that primarily controls vegetative functions during rest, relaxation, and digestion. It is responsible for the body's "rest and digest" activities including decreasing heart rate, lowering blood pressure, increasing digestive activity, and stimulating sexual arousal. The PNS utilizes acetylcholine as its primary neurotransmitter and acts in opposition to the Sympathetic Nervous System (SNS), which is responsible for the "fight or flight" response.

Guanabenz is not a medical condition, it's a medication. Here's the definition:

Guanabenz (brand name Wytensin) is a centrally acting antihypertensive agent, primarily used for the treatment of hypertension. It belongs to the class of drugs known as "central alpha-2 adrenergic agonists." Guanabenz works by mimicking the effects of natural neurotransmitters in your body to reduce nerve impulses that cause blood vessels to constrict, thereby promoting vasodilation and lowering blood pressure.

Please consult a healthcare professional or refer to medical resources for more detailed information about specific medications and their uses, side effects, and interactions.

Alpha-Methyltyrosine (α-MT) is a synthetic amino acid that acts as an inhibitor of the enzyme tyrosine hydroxylase. This enzyme is a rate-limiting step in the biosynthesis of catecholamines, including neurotransmitters such as dopamine and norepinephrine. By inhibiting tyrosine hydroxylase, α-MT reduces the synthesis of these catecholamines, which can lead to various effects on the nervous system.

In medical contexts, α-MT has been used in research settings to study the functions of catecholamines and their role in various physiological processes. It has also been investigated as a potential treatment for certain conditions, such as hypertension and anxiety disorders, although its clinical use is not widespread due to its side effects and limited efficacy.

It's important to note that α-MT should only be used under the supervision of a medical professional, as it can have significant effects on the nervous system and may interact with other medications or health conditions.

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.

In contrast, yohimbine is a pure alkaloid that can be isolated from yohimbe bark. Yohimbine is just one of at least 55 indole ... Yohimbine interacts with serotonin and dopamine receptors in high concentrations. Yohimbine has been studied as a way to ... "Yohimbine (PIM 567)". Inchem.org. Retrieved 2013-05-26. "Yohimbine". DrugBank. University of Alberta. Archived from the ... In contrast, there is a "fairly rich literature on yohimbine". Subsequent work on yohimbine, while confirming that it behaves ...
"Yohimbine". DrugBank. Archived from the original on 30 January 2013. Retrieved 12 February 2013. Fattorusso, p. 53 Thomas ... including morphine and yohimbine are very slightly water-soluble (0.1-1 g/L). Alkaloids and acids form salts of various ...
"Yohimbine (PIM 567)". Inchem.org. Retrieved 2013-05-26. Winsauer PJ, Rodriguez FH, Cha AE, Moerschbaecher JM (January 1999). " ... Arthur JM, Casañas SJ, Raymond JR (June 1993). "Partial agonist properties of rauwolscine and yohimbine for the inhibition of ... Kaumann AJ (June 1983). "Yohimbine and rauwolscine inhibit 5-hydroxytryptamine-induced contraction of large coronary arteries ... Tiospirone Trazodone Trifluoromethylphenylpiperazine Trimethoxyamphetamine Umespirone Urapidil Vilazodone Xaliproden Yohimbine ...
Tam, S. W.; Worcel, M.; Wyllie, M. (2001-09-01). "Yohimbine: a clinical review". Pharmacology & Therapeutics. 91 (3): 215-243. ... Phenoxybenzamine Phentolamine Prazosin Tamsulosin Yohimbine Propranolol Timolol Atenolol Metoprolol Butaxamine Still under ...
Yohimbine Piperazines: DBL-583 • GBR-12,935 • Nefazodone • Vanoxerine Piperidines: 1-(1-(1-Benzothiophen-2-yl)cyclohexyl) ...
He led a team who were the first persons to achieve the total synthesis of yohimbine. He pioneered in what is today called ... "The Total Synthesis of Yohimbine". J. Am. Chem. Soc. 80 (18): 5006-5007. doi:10.1021/ja01551a062. E. E. van Tamelen "The Role ...
Jacobsen, E. N.; Dustin, J. M.; Zuend, S. J. (November 2008). "Catalytic asymmetric total synthesis of (+)-Yohimbine". Org. ... In the Jacobsen synthesis of (+)-yohimbine, an indole alkaloid, an early enantioselective Pictet-Spengler reaction using a ...
Ajmalicine Corynanthine Spegatrine Yohimbine KOHLI JD, DE NN (June 1956). "Pharmacological action of rauwolscine". Nature. 177 ... Arthur JM, Casañas SJ, Raymond JR (June 1993). "Partial agonist properties of rauwolscine and yohimbine for the inhibition of ... Rauwolscine, also known as isoyohimbine, α-yohimbine, and corynanthidine, is an alkaloid found in various species within the ... Perry BD, U'Prichard DC (December 1981). "[3H]rauwolscine (alpha-yohimbine): a specific antagonist radioligand for brain alpha ...
... , also known as δ-yohimbine or raubasine, is an antihypertensive drug used in the treatment of high blood pressure. ... Ajmalicine is structurally related to yohimbine, rauwolscine, and other yohimban derivatives. Like corynanthine, it acts as a ... Corynanthine Rauwolscine Spegatrine Yohimbine Wink, Michael; Roberts, M. W. (1998). Alkaloids: biochemistry, ecology, and ...
Yohimbine was used for the treatment of erectile dysfunction in men until emergence of more efficient drugs. Some alkaloids ... Yohimbine is more selective to α2 adrenoceptor; by blocking presynaptic α2-adrenoceptors, it increases the release of ... Strictosidine Catharanthine Yohimbine Vinca Strychnine Ellipticine There are also purely structural classifications based on ...
Total synthesis of (±)-reserpine and (±)-α-yohimbine". Journal of the American Chemical Society. 109 (20): 6124-6134. doi: ...
... yohimbine (Procomil; a tryptamine alkaloid found in Pausinystalia johimbe) Alcohol: "Euphoria, the feeling of well-being, has ... yohimbine and corynanthine many others Fungi: psilocybin mushrooms: psilocybin and psilocin various Amanita mushrooms: muscimol ...
Yohimbine has been shown to be effective in the treatment of orgasmic dysfunction in men. Meditation has demonstrated ... Adeniyi AA, Brindley GS, Pryor JP, Ralph DJ (May 2007). "Yohimbine in the treatment of orgasmic dysfunction". Asian Journal of ...
The NIH states that yohimbine hydrochloride has been shown in human studies to be possibly effective in the treatment of male ... Retrieved 13 December 2010.[dead link] Adeniyi AA, Brindley GS, Pryor JP, Ralph DJ (May 2007). "Yohimbine in the treatment of ... Cyproheptadine, buspirone, stimulants such as amphetamines (including the antidepressant bupropion), nefazodone and yohimbine ...
Conophylline Vobtusine Rauwolscine Yohimbine Dewick, Paul M (2002). Medicinal Natural Products. A Biosynthetic Approach. Second ...
For instance, Yohimbine has been used to treat sexual dysfunction in males. However, the effectiveness of this medication for ... Examples of alpha 2 blockers include yohimbine and idazoxan. Apart from being used as antidotes to reverse the overdose effects ...
Like yohimbine and rauwolscine, corynanthine has also been shown to possess some activity at serotonin receptors. Ajmalicine ... Dual effects of yohimbine, rauwolscine and corynanthine as alpha-adrenoceptor antagonists and 5-HT-receptor agonists". Naunyn- ... This is in contrast to yohimbine and rauwolscine which have around 30-fold higher affinity for the α2-adrenergic receptor over ... It is one of the two diastereoisomers of yohimbine, the other being rauwolscine. It is also related to ajmalicine. Corynanthine ...
Yohimbine, an α2 blocker derived from the bark of the Pausinystalia johimbe tree, has been tested to increase libido and treat ... Yohimbine can interact with stimulants, hypertension drugs, naloxone, and clonidine. Interactions with such drugs can cause ... Conversely, α2 blockers, such as Yohimbine, appear to provide significant improvement of the sclerotic symptoms in Raynaud's ... Alpha blockers that may have these side effects include yohimbine, phenoxybenzamine, and phentolamine. When alpha blockers are ...
"Erowid Yohimbe Vaults : Notes on Yohimbine by William White, 1994". Erowid.org. Archived from the original on 2013-01-26. ...
Bavadekar SA, Ma G, Mustafa SM, Moore BM, Miller DD, Feller DR (November 2006). "Tethered yohimbine analogs as selective human ... 2-phenoxy-nicotinamide Quetiapine Risperidone Spiroxatrine Yohimbine derivatives 9 and 10: >43 fold selectivity over α2A, α2B ...
Yohimbine specifically has so been declared by the European Union, but not by the US National Institutes of Health.[additional ... The main phytochemical in the extract is the indoloquinolizidine alkaloid yohimbine. It also contains other alkaloids, such as ... and yohimbine levels may vary substantially among supplement products. Although proposed as a potential treatment for erectile ... citation(s) needed] Coffea Mitragyna speciosa List of herbs with known adverse effects Yohimbine "Corynanthe johimbe K.Schum ...
Lipokinetix also contained norephedrine (PPA), caffeine, yohimbine and 3,5-diiodothyronine. Usnic acid has been found to have ... The product contains norephedrine (also known as phenylpropanolamine or PPA), caffeine, yohimbine, diiodothyronine, and sodium ...
Ajmalicine Corynanthine Deserpidine Mitragynine Rauwolscine Spegatrine Reserpine Rescinnamine Yohimbine Elisabetsky, E; Costa- ...
Yohimbine, historically used as an aphrodisiac, is sometimes used in veterinary medicine (although now largely replaced by ... yohimbine, and rauwolscine, phentolamine. Lemke, KA (June 2004). "Perioperative use of selective alpha-2 agonists and ...
Cohen PA, Wang YH, Maller G, DeSouza R, Khan IA (March 2016). "Pharmaceutical quantities of yohimbine found in dietary ... Some botanical supplements include high dosages of compounds found in plants with stimulant effects including yohimbine and ...
Alpha-2 antagonists such as atipamezole and yohimbine may be used to reverse the effects of xylazine in animals. Side-effects ... Ndeereh DR, Mbithi PM, Kihurani DO (June 2001). "The reversal of xylazine hydrochloride by yohimbine and 4-aminopyridine in ... Murahata Y, Miki Y, Hikasa Y (October 2014). "Antagonistic effects of atipamezole, yohimbine, and prazosin on xylazine-induced ... Janssen CF, Maiello P, Wright MJ, Kracinovsky KB, Newsome JT (March 2017). "Comparison of Atipamezole with Yohimbine for ...
Yohimbine, harmine, harmaline and ajmalicine occurs in descending order, yohimbine being highest. The tobacco plant readily ...
Yohimbine can be used as an antidote to rapidly reverse the effects. Spadavecchia C, Arendt-Nielsen L, Andersen OK, ...
For example, one of the common reported side effects of the intake of yohimbine is piloerection. Piloerection is one of the ... Goldberg, M R (1983). "Influence of yohimbine on blood pressure, autonomic reflexes, and plasma catecholamines in Humans". ...
Petrash AC, Bylund DB (Jun 1986). "Alpha-2 adrenergic receptor subtypes indicated by [3H]yohimbine binding in human brain". ... Agonists (−)-Dibromophakellin Antagonists Imiloxan Yohimbine Adrenergic receptor GRCh38: Ensembl release 89: ENSG00000274286 - ...

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