ISSN:
1474-8673
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Chemistry and Pharmacology
,
Medicine
Notes:
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 μm) elicited concentration-dependent relaxation of precontracted (1 μm 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 μm). 3 SNP-mediated relaxations were almost abolished by 10 μm ryanodine. 4 SNP-mediated relaxations were also reduced by either 1 μm apamin (a selective small conductance Ca2+-sensitive K+ channel, SKCa, inhibitor) or the selective L-type Ca2+ channel inhibitor, nicardipine (3 μm). 5 SNP-induced relaxations were insensitive to 1 mm tetraethylammonium chloride (an inhibitor of large-conductance Ca2+-sensitive K+ channels) and 1 μm 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1046/j.1474-8673.2002.00271.x
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