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A2-receptor adrenergic

Cionidine. Clonidine dampens sympathetic activity originating at the locus coeruleus by stimulation of presynaptic a2-adrenergic receptors in the sympathetic chain (Covey and Classman 1991 Hughes 1994). It appears to have some efficacy for alcohol and opioid withdrawal and thus was evaluated for treatment of nicotine withdrawal as well (Covey and Classman 1991 Hughes 1994). Several clinical trials used oral or transdermal clonidine in doses of 0.1—0.4 mg/day for 2—6 weeks with or without behavior therapy. Three meta-analytic reviews reported that clonidine improved quit rates (Covey and Classman 1991 Courlay and Benowitz 1995 Law and Tang 1995). [Pg.326]

Monoamine oxidase inhibition Serotonin reuptake inhibition Norepinephrine reuptake inhibition Dopamine reuptake inhibition a2-Adrenergic receptor blockade Serotonin-2A receptor blockade Serotonin-2C receptor blockade Serotonin-3 receptor blockade op-Adrenergic receptor blockade Histamine-1 receptor blockade Muscarinic cholinergic receptor blockade... [Pg.573]

Yohimbine is an indole alkaloid produced in the bark of yohimbe trees. It selectively inhibits a2-adrenergic receptors in the brain that are associated with libido and penile erection. Since there is only limited data supporting its efficacy, yohimbine is not a recommended treatment for any form of ED.22 Adverse effects of the drug include nausea, irritability, headaches, anxiety, tachycardia, and hypertension. [Pg.787]

Prazosin is a selective aradrenergic receptor antagonist that, at therapeutic doses, has little activity at a2-adrenergic receptors and clinically insignificant direct vasodilating activity The drug does not cause the other effects attributed to phentolamine. Most important, it produces less tachycardia than does phentolamine and, therefore, is useful in the treatment of essential hypertension. [Pg.191]

A further consideration is that receptors which primarily activate one pathway may, on occasion, activate a second pathway (Fig. 10-10). An example is the ability of GPCRs, such as a2-adrenergic receptors or mAChRs, to activate the MAPK cascade. Activation of adenylyl cyclase-linked receptors results in the release of G protein Py subunits, which, probably via an intermediary protein tyrosine kinase (PTK-X), stimulates phosphorylation of the adaptor protein SHC [36]. This in turn recruits the Grb2-SOS complex and activates the MAPK pathway. [Pg.180]

The postsynaptic receptors on any given neuron receive information from transmitters released from another neuron. Typically, postsynaptic receptors are located on dendrites or cell bodies of neurons, but may also occur on axons or nerve terminals in the latter case, an axoaxonic synaptic relationship may cause increases or decreases in transmitter release. In contrast, autoreceptors are found on certain neurons and respond to transmitter molecules released from the same neuron. Autoreceptors may be widely distributed on the surface of the neuron. At the nerve terminal, they respond to transmitter molecules released into the synaptic cleft on the cell body, they may respond to transmitter molecules released by dendrites. Functionally, most autoreceptors appear to decrease further transmitter release in a kind of negative feedback loop. Autoreceptors have been identified for all the catecholamines, as well as for several other neurotransmitters. a2-adrenergic receptors are often found on noradrenergic nerve terminals of postganglionic sympathetic nerves, as well as on noradrenergic neurons in the CNS [36], and activation of these receptors decreases further norepinephrine release. Dopamine autoreceptors,... [Pg.218]

More direct evidence of noradrenergic effects comes from studies using the a2 antagonist, yohimbine. a2 adrenergic receptors are known to be present on the cell bodies and terminals of norepinephrine neurons,... [Pg.902]

Clonidine, guanabenz, guanfacine, and methyldopa lower BP primarily by stimulating a2-adrenergic receptors in the brain, which reduces sympathetic outflow from the vasomotor center and increases vagal tone. Stimulation of presynaptic oq-receptors peripherally may contribute to the reduction in sympathetic tone. Consequently, there may be decreases in heart rate, cardiac output, total peripheral resistance, plasma renin activity, and baroreceptor reflexes. [Pg.135]

Transgenic Models of a2-Adrenergic Receptor Subtype Function... [Pg.161]

Three genes encoding for a2-adrenergic receptor subtypes have been identified from several species, termed a2A. and a2c, respectively (Fig. 1, 2). [Pg.163]

Fig. 2. a2-Adrenergic receptor subtypes. The putative membrane topology of the three mouse a2-receptor subtypes is schematically depicted. Open circles represent amino acids which are identical between all subt es, gray circles represent amino acids which are conserved among two subtypes, dark circles are non-identical amino acids. Tissue distribution of tt2-receptor subtypes is based on mRNA and protein expression references are given in the text... [Pg.163]

Fig. 5. In vivo functions of a2-adrenergic receptor subtypes. This overview assigns physiological effects of a2-receptor stimulation to individual a2-receptor subtypes iDased on experiments performed in transgenic mice carrying deletions in a2-receptor gene (see text for references)... Fig. 5. In vivo functions of a2-adrenergic receptor subtypes. This overview assigns physiological effects of a2-receptor stimulation to individual a2-receptor subtypes iDased on experiments performed in transgenic mice carrying deletions in a2-receptor gene (see text for references)...
Eason MG, Jacinto MT, Liggett SB (1994) Contribution of ligand structure to activation of a2-adrenergic receptor subtype coupling to G,. Molec Pharmacol 45 696-702... [Pg.180]


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See also in sourсe #XX -- [ Pg.90 ]

See also in sourсe #XX -- [ Pg.354 ]




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