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Ai-Adrenergic receptors

Cotecchia S et al (2004) Structural determinants involved in the activation and regulation of G protein-coupled receptors lessons from the ai -adrenergic receptor sub-types. Biol Cell 96 327-333... [Pg.45]

Piascik MT, Perez DM (2007) Structure-function of ai-adrenergic receptors. Biochem Phannacol 73 1051-1062... [Pg.45]

Lopez-Rodriguez, M.L., Morcillo, M.J., Fernandez, E., Porras, E., Orensanz, L., Beneytez, M.E., Manzanares, J. and Fuentes, J.A. (2001) Synthesis and structure-activity relationships of a new model of arylpiperazines. 5. Study of the physicochemical influence of the pharmacophore on 5-HT]A/ai-adrenergic receptor affinity. Synthesis of a new selective derivative with mixed 5-HT1A/D2 antagonist properties. Journal of Medicinal Chemistry, 44, 186-197. [Pg.475]

Binds to DNA and prevents separation of the helical strands Affects neuronal transmissions Binds to opiate receptors and blocks pain pathway Acts as central nervous system depressant Inhibits Na/K/ATPase, increases intracellular calcium, and increases ventricular contractibility Blocks the actions of histamine on Hi receptor Blocks ai-adrenergic receptor, resulting in decreased blood pressure Inhibits reuptake of 5-hydroxytryptamine (serotonin) into central nervous system neurons Inhibits cyclooxygenase, inhibition of inflammatory mediators Inhibits replication of viruses or tumor cells Inhibits HIV reverse transcriptase and DNA polymerase Antagonizes histamine effects... [Pg.412]

CPCR Anti-target Pharmacophore Modeling the ai Adrenergic Receptor 289... [Pg.289]

Michelotti GA, Price DT, Schwinn DA (2000) ai-adrenergic receptor regulation basic science and clinical implications. Pharmacol Ther 88 281-309 Miller RJ (1998) Presynaptic receptors. Annu Rev Pharmacol Toxicol 38 201-27 Mishima K, Tanoue A, Tsuda M, Hasebe N, Fukue Y, Egashira N, Takano Y, Kamiya HO, Tsu-jimoto G, Iwasaki K, Fujiwara M (2004) Characteristics of behavioral abnormalities in ocid-adrenoceptors deficient mice. Behav Brain Res 152 365-73 Miyakawa T, Yamada M, Duttaroy A, Wess J (2001) Hyperactivity and intact hippocampus-dependent learning in mice lacking the Mi muscarinic acetylcholine receptor. J Neurosci 21 5239-50... [Pg.284]

Piasdk MT, Perez DM (2001) ai-adrenergic receptors new insights and directions. J Exp Pharmacol Ther 298 403-10... [Pg.285]

Hampel C, Dolber PC, Smith MP, et al. Modulation of bladder ai-adrenergic receptor subtype expression by bladder outlet obstruction. J Urol 2002 167 1513-1521. [Pg.145]

Venlafaxine, a stmcturally novel antidepressant, is a potent inhibitor of 5-HT and NE renptake and a weak inhibitor of dopamine reuptake. Unlike the TCAs, it has virtnaUy no affinity for mnscarinic, histaminergic, and ai-adrenergic receptors. ... [Pg.1239]

Second-generation agents include prazosin, terazosin, doxazosin, and alfuzosin. These differ in terms of duration of action and dosing schedule. Whereas prazosin requires dosing two to three times a day, terazosin, doxazosin, and alfuzosin offer more convenient once-daUy dosing. Prazosin, terazosin, and doxazosin antagonize peripheral vascular ai-adrenergic receptors, in addition to those in the prostate, at the usual doses used to treat BPH. As a result, first-dose syncope, orthostatic hypotension, and dizziness are... [Pg.1541]

Doxazosin a-Adrenergic blocker, Blocks ai-adrenergic receptor,... [Pg.328]

Gia Adenylyl cyclase channel (Gp., activates effector) cAMP (decreased) Change in membrane potential ai-Adrenergic receptor Muscarinic acetylcholine receptor... [Pg.545]

They block ai-adrenergic receptors in veins and arterioles, thereby causing vasodilation and decreased peripheral vascular resistance. As a result, blood pressure is reduced. An example is doxazosin. [Pg.67]

Kurz T., Schneider I., Tolg R., Richardt G. ai-adrenergic receptor-mediated increase in the mass of phosphatidic acid and 1,2-diacylglycerol in ischemic rat heart. Cardiovasc. Res. 42... [Pg.319]

Between 1960 and 1980, TCAs were the major pharmacological treatment for depression (18). The TCAs, however, have many other actions in addition to blocking monoamine reuptake, including anticholinergic, antihistaminergic, and cardiotoxic side effects that are related to their affinity for muscarinic, histamine, and ai-adrenergic receptors as well as their action on cardiac and central... [Pg.805]

The family of TCAs has many undesirable side effects and behaves like five drugs wrapped into one. They not only block the reuptake of NE and 5-HT but also block muscarinic receptors (anticholinergic), ai-adrenergic receptors, Hi-receptors (antihistamine), and sodium channels. The common side effects and appropriate responses are given in Table 21.4. [Pg.825]

Photaffinity Probes for the ai-Adrenergic Receptor and the Calcium Channel Bind to a Common Domain in P-Glycoprotein. [Pg.402]

See other pages where Ai-Adrenergic receptors is mentioned: [Pg.42]    [Pg.43]    [Pg.43]    [Pg.7]    [Pg.191]    [Pg.506]    [Pg.94]    [Pg.280]    [Pg.85]    [Pg.42]    [Pg.43]    [Pg.43]    [Pg.469]    [Pg.208]    [Pg.121]    [Pg.364]    [Pg.366]    [Pg.824]    [Pg.825]    [Pg.846]    [Pg.864]    [Pg.1147]    [Pg.2019]    [Pg.181]    [Pg.926]   
See also in sourсe #XX -- [ Pg.90 ]



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