Abstract:
:We tested the hypothesis that relaxation of the rat mesenteric artery in response to insulin is mediated by K(+) channels. Two concentrations of insulin (10 and 100 mU/ml) induced relaxation of the artery by 6+/-1%, 24+/-3% (mean+/-S.E.M.). Denudation of the endothelium or precontraction by KCl (30 mM), clotrimazole (10 microM), a cytochrome P450 inhibitor, charybdotoxin (30 nM) an inhibitor of large-conductance Ca(2+)-activated K(+) channels, abolished the relaxation of the artery in response to insulin. However, N(omega)-nitro-L-arginine methyl ester (L-NAME; 100 microM), an inhibitor of nitric oxide synthase, apamin (1 microM), an inhibitor of small-conductance Ca(2+)-activated K(+) channels, or glibenclamide (10 microM), an ATP-sensitive K(+) channels blocker, did not attenuate the relaxation of the artery caused by insulin. These results suggest that the relaxation of rat mesenteric artery in response to insulin is mediated mostly by large-conductance Ca(2+)-activated K(+) channels, perhaps an endothelium-derived hyperpolarizing factor (EDHF).
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Iida S,Taguchi H,Watanabe N,Kushiro T,Kanmatsuse Kdoi
10.1016/s0014-2999(00)00892-xkeywords:
subject
Has Abstractpub_date
2001-01-05 00:00:00pages
155-160issue
1-2eissn
0014-2999issn
1879-0712pii
S0014-2999(00)00892-Xjournal_volume
411pub_type
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