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Postsynaptic alpha-adrenoceptor antagonists

POSTSYNAPTIC ALPHA-ADRENOCEPTOR ANTAGONISTS fSEDA-33, 425 SEDA-34, 330 SEDA-35, 377J ... [Pg.286]

Alpha-adrenoceptor antagonists inhibit the activation of a adrenoceptors by catecholamines. In the cardiovascular system these receptors are mainly located on the surface of smooth muscle cells in the walls of arteries and veins. On activation, they mediate an increase in intracellular free calcium, which induces smooth muscle contraction. Inhibition by an a antagonist causes arterial or venous vasodilatation. The postsynaptic effect is mainly mediated by ol adrenoceptors whereas o2 adrenoceptors are found on the presynaptic membranes of the sympathetic neurones. Activation of o2-adreno-ceptors results in auto-inhibition of catecholamine release. [Pg.140]

Trazodone (SEDA-7,19-21) is a triazolopyridine derivative that selectively but weakly inhibits 5-hydroxytrypta-mine (5-HT) re-uptake and is an alpha-adrenoceptor antagonist at both presynaptic and postsynaptic receptors (1). During long-term administration it down-regulates serotonin receptors (2). [Pg.110]

Indoramin is a postsynaptic selective alphai-adrenoceptor antagonist that is chemically distinct from the quinazo-lines. Unlike some other alpha-blockers, indoramin lowers blood pressure without a resulting reflex tachycardia or postural hypotension (1). However, it has largely been supplanted by more modern drugs, such as doxazosin, prazosin, and terazosin. [Pg.1746]


See other pages where Postsynaptic alpha-adrenoceptor antagonists is mentioned: [Pg.16]    [Pg.28]   


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Alpha-adrenoceptor antagonists

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