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Department of Physiology, School of Medicine, University of Maryland, Baltimore, Maryland 21201
Submitted 13 November 2003 ; accepted in final form 25 March 2004
The possible roles of endothelial intracellular Ca2+ concentration ([Ca2+]i), nitric oxide (NO), arachidonic acid (AA) metabolites, and Ca2+-activated K+ (KCa) channels in adrenergically induced vasomotion were examined in pressurized rat mesenteric arteries. Removal of the endothelium or buffering [Ca2+]i selectively in endothelial cells with BAPTA eliminated vasomotion in response to phenylephrine (PE; 10.0 µM). In arteries with intact endothelium, inhibition of NO synthase with N
-nitro-L-arginine methyl ester (L-NAME; 300.0 µM) or N-nitro-L-arginine (L-NNA; 300.0 µM) did not eliminate vasomotion. Neither inhibition of cGMP formation with 10.0 µM 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) nor inhibition of prostanoid formation (10.0 µM indomethacin) eliminated vasomotion. Similarly, inhibition of AA cytochrome P-450 metabolism with an intraluminal application of 17-octadecynoic acid (17-ODYA) or 6-(2-propargyloxyphenyl)hexanoic acid (PPOH) failed to eliminate vasomotion. In contrast, intraluminal application of the KCa channel blockers apamin (250.0 nM) and charybdotoxin (100.0 nM), together, abolished vasomotion and changed synchronous Ca2+ oscillations in smooth muscle cells to asynchronous propagating Ca2+ waves. Apamin, charybdotoxin, or iberiotoxin (100.0 nM) alone did not eliminate vasomotion, nor did the combination of apamin and iberiotoxin. The results show that adrenergic vasomotion in rat mesenteric arteries is critically dependent on Ca2+-activated K+ channels in endothelial cells. Because these channels (small- and intermediate-conductance KCa channels) are a recognized component of EDHF, we conclude therefore that EDHF is essential for the development of adrenergically induced vasomotion.
smooth muscle; endothelial cell; Ca2+
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