Effects of putative K+ channel blockers on β-adrenoceptor-mediated vasorelaxation of rat mesenteric artery

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journalpeer-review

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Original languageEnglish
Pages (from-to)515-519
Journal / PublicationJournal of Cardiovascular Pharmacology
Issue number4
Publication statusPublished - Apr 1997
Externally publishedYes


The aim of our study was to investigate the contribution of Ca2+ activated K+ channels (K(Ca) channels) and ATP-sensitive K+ channels (K(ATP) channels) to the vasodilator responses to β-adrenoceptor agonists in the rat isolated mesenteric artery. Isoprenaline and fenoterol concentration- dependently relaxed the phenylephrine-precontracted endothelium-intact arterial rings with 50% inhibitory concentration (IC50) of 0.0314 ± 0.027 μM (n = 20) and 0.40 ± 0.04 μM (n = 11), respectively. Charybdotoxin (100 nM) displaced the isoprenaline or fenoterol logarithmic concentration- relaxation curve to the right in the absence and presence of endothelium. In contrast, glibenclamide (10 μM) did not affect the effects of isoprenaline and fenoterol, whereas glibenclamide (3 μM) significantly inhibited the cromakalim-induced vasorelaxation. Neither charybdotoxin (100 nM) nor glibenclamide (10 μM) influenced the vasorelaxation induced by forskolin. Ba2+, a nonselective blocker of K+ channels, inhibited the relaxant effects of isoprenaline and forskolin. These results suggest that K(Ca) but not K(ATP) channels contribute to β-adrenoceptor-mediated vasodilator response in rat mesenteric artery, and cyclic adenosine monophosphate (cAMP) might not be involved in regulation of the activity of K(Ca) channels.

Research Area(s)

  • β-Adrenoceptor, Charybdotoxin, Glibenclamide, K+ channel, Mesenteric artery, Rat, Vasorelaxation

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