3-morpholinosydnonimine (SIN-1) and K+ channels in smooth muscle cells of the rabbit and guinea pig carotid arteries

Citation
Jf. Quignard et al., 3-morpholinosydnonimine (SIN-1) and K+ channels in smooth muscle cells of the rabbit and guinea pig carotid arteries, EUR J PHARM, 399(1), 2000, pp. 9-16
Citations number
25
Categorie Soggetti
Pharmacology & Toxicology
Journal title
EUROPEAN JOURNAL OF PHARMACOLOGY
ISSN journal
00142999 → ACNP
Volume
399
Issue
1
Year of publication
2000
Pages
9 - 16
Database
ISI
SICI code
0014-2999(20000630)399:1<9:3(AKCI>2.0.ZU;2-B
Abstract
Experiments were designed to determine the subtype of K+ channels activated by the nitrovasodilator 3-morpholinosydnonimine (SIN-1) in smooth muscle c ells of the rabbit and guinea pig carotid arteries. Membrane potential was recorded in isolated segments with intracellular microelectrode and K+ curr ents in freshly dissociated smooth muscle cells, with the patch-clamp techn ique. In the guinea pig carotid artery, SIN-1 caused a glibenclamide-sensit ive hyperpolarization. The nitrovasodilator did not affect the whole-cell K + current, but activated a glibenclamide-sensitive K+ current. In the rabbi t carotid artery, SIN-1 induced only an iberiotoxin-sensitive repolarizatio n in phenylephrine-depolarized tissue and in isolated cells, enhanced the a ctivity of an iberiotoxin-sensitive K+ current. These findings demonstrate that the population of K+ channels activated by nitric oxide (NO) is specie s-dependent and support the conclusion that, in the guinea pig carotid arte ry, in contrast to the rabbit carotid artery, the release of NO cannot acco unt for the responses attributed to endothelium-derived hyperpolarizing fac tor (EDHF). (C) 2000 Elsevier Science B.V. All rights reserved.