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Inhibition of voltage-dependent Ca(2+)-current by alpha-adrenoceptor agonists in smooth muscle cells.

Abstract：

:The cellular mechanisms underlying the inhibitory effects of phenylephrine on dihydropyridine-sensitive, voltage-dependent Ca2+ currents recorded from single smooth muscle cells dissociated from the rat anococcygeus muscle were examined. Phenylephrine (0.1-30 microM) produced a concentration-dependent inhibition of the Ca2+ current; the maximum response occurred at a concentration of 10 microM, which inhibited the peak inward current evoked at 0 mV by 57.7 +/- 4% (n = 8). The response to phenylephrine was reduced but not abolished in cells containing 1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid (BAPTA; 10 mM), and it persisted in cells dialysed internally with heparin (5 mg.ml-1). This was despite the fact that both EGTA (5 mM) and heparin were able to block the phenylephrine-induced, Ca(2+)-dependent chloride current recorded in the same cells. The inhibition of the Ca2+ current produced by phenylephrine was abolished in cells containing guanosine 5'-[beta-thio]diphosphate (GDP-beta-S) but persisted in cells pre-treated with pertussis toxin. Our results suggest that the inhibition of L-type Ca2+ current seen following alpha-adrenoceptor activation occurs by a mechanism independent from the inositol trisphosphate-mediated release of Ca2+ from intracellular stores.

journal_name

Eur J Pharmacol

journal_title

European journal of pharmacology

authors

England S,McFadzean I

doi

10.1016/0922-4106(95)90049-7

subject

Has Abstract

pub_date

1995-02-15 00:00:00

pages

355-64

issue

3

eissn

0014-2999

issn

1879-0712

journal_volume

288

pub_type

杂志文章

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