Role of K+ channels in N-acetylprocainamide-induced relaxation of bovine tracheal smooth muscle.
Eur J Pharmacol
; 415(1): 73-8, 2001 Mar 09.
Article
em En
| MEDLINE
| ID: mdl-11245854
ABSTRACT
We examined the relaxant effects of N-acetylprocainamide, the major hepatic metabolite of procainamide, on bovine tracheal smooth muscle, focusing on the possible involvement of K+ channels. N-acetylprocainamide produced a concentration-dependent and full inhibition of the tension development elicited by methacholine (0.3 or 1 microM). The potency of N-acetylprocainamide in diminishing methacholine-elicited tension development was one-half of that of procainamide. By comparison, N-acetylprocainamide inhibited high-K+ (40 mM)-induced contraction more potently than procainamide though both inhibitions were largely reduced when compared to those against methacholine-induced contraction. Iberiotoxin (30 nM), Ba(2+) (1 mM) or a combination of both agents significantly attenuated the relaxant effect of N-acetylprocainamide on methacholine-induced contraction, whereas apamin (100 nM), 4-aminopyridine (300 microM), and glibenclamide (10 microM) did not affect it. These results suggest that N-acetylprocainamide, similar to procainamide, elicits tracheal smooth muscle relaxation mainly through the activation of plasma membrane K+ channels.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Acecainida
/
Traqueia
/
Canais de Potássio
/
Relaxamento Muscular
/
Músculo Liso
Limite:
Animals
Idioma:
En
Ano de publicação:
2001
Tipo de documento:
Article