Sodium nitroprusside-induced rat fundus relaxation is ryanodine-sensitive and involves L-type Ca2+ channel and small conductance Ca(2+)-sensitive K+ channel components.
Auton Autacoid Pharmacol
; 22(5-6): 297-301, 2002.
Article
em En
| MEDLINE
| ID: mdl-12866810
ABSTRACT
1 The aim of this study was to examine whether sodium nitroprusside (SNP)-induced relaxation of rat fundus longitudinal smooth muscle involves ryanodine-sensitive Ca2+ release. 2 SNP (300 nM-30 microM) elicited concentration-dependent relaxation of precontracted (1 microM carbachol) rat fundus, an effect almost abolished by the selective guanylyl cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one (ODQ, 10 microM). 3 SNP-mediated relaxations were almost abolished by 10 microM ryanodine. 4 SNP-mediated relaxations were also reduced by either 1 microM apamin (a selective small conductance Ca(2+)-sensitive K+ channel, SKCa, inhibitor) or the selective L-type Ca2+ channel inhibitor, nicardipine (3 microM). 5 SNP-induced relaxations were insensitive to 1 mM tetraethylammonium chloride (an inhibitor of large-conductance Ca(2+)-sensitive K+ channels) and 1 microM glibenclamide (an ATP-sensitive K+ channel inhibitor). 6 These data suggest that SNP-mediated fundus relaxation occurs via a cGMP-mediated and ryanodine-sensitive mechanism which requires, at least in part, SKCa and L-type Ca2+ channel activity.
Buscar no Google
Bases de dados:
MEDLINE
Assunto principal:
Rianodina
/
Nitroprussiato
/
Canais de Cálcio Tipo L
/
Canais de Potássio Cálcio-Ativados
/
Músculo Liso
Tipo de estudo:
Diagnostic_studies
Limite:
Animals
Idioma:
En
Revista:
Auton Autacoid Pharmacol
Assunto da revista:
FARMACOLOGIA
/
NEUROLOGIA
Ano de publicação:
2002
Tipo de documento:
Article
País de afiliação:
Reino Unido