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Contribution of α ‐adrenoceptors to depolarization and contraction evoked by continuous asynchronous sympathetic nerve activity in rat tail artery
Author(s) -
Brock J. A.,
Mclachlan E. M.,
Rayner S. E.
Publication year - 1997
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0701055
Subject(s) - prazosin , depolarization , idazoxan , contraction (grammar) , phenylephrine , medicine , nifedipine , muscle contraction , endocrinology , antagonist , myogenic contraction , chemistry , biophysics , biology , calcium , smooth muscle , receptor , blood pressure
The effects of continuous but asynchronous nerve activity induced by ciguatoxin (CTX‐1) on the membrane potential and contraction of smooth muscle cells have been investigated in rat proximal tail arteries isolated in vitro . These effects have been compared with those produced by the continuous application of phenylephrine (PE). CTX‐1 (0.4 n m ) and PE (10 μ m ) produced a maintained depolarization of the arterial smooth muscle that was almost completely blocked by α‐adrenoceptor blockade. In both cases, the depolarization was more sensitive to the selective α 2 ‐adrenoceptor antagonist, idazoxan (0.1 μ m ), than to the selective α 1 ‐adrenoceptor antagonist, prazosin (0.01 μ m ). In contrast, the maintained contraction of the tail artery induced by CTX‐1 (0.2 n m ) and PE (2 and 10 μ m ) was more sensitive to prazosin (0.01) μ m , than to idazoxan (0.01 μ m ). In combination, these antagonists almost completely inhibited contraction to both agents. Application of the calcium channel antagonist, nifedipine (1 μ m ), had no effect on the depolarization induced by either CTX‐1 or PE but maximally reduced the force of the maintained contraction to both agents by about 50%. We conclude that the constriction of the tail artery induced by CTX‐1, which mimics the natural discharge of postganglionic perivascular axons, is due almost entirely to α‐adrenoceptor activation. The results indicate that neuronally released noradrenaline activates more than one α‐adrenoceptor subtype. The depolarization is dependent primarily on α 2 ‐adrenoceptor activation whereas the contraction is dependent primarily on α 1 ‐adrenoceptor activation. The links between α‐adrenoceptor activation and the voltage‐dependent and voltage‐independent mechanisms that deliver Ca 2+ to the contractile apparatus appear to be complex.British Journal of Pharmacology (1997) 120 , 1513–1521; doi: 10.1038/sj.bjp.0701055