Adenosine a2-receptor mediates ethanol-induced arteriolar dilation
in the rat stomach.
Nagata, Hiroshi, Eiichi Sekizuka, Tetsuo Morishita, Masayuki
Tatemichi, Tsuyoshi Kurokawa, Akira Mizuki, and Hiromasa Ishii.
Department of Internal Medicine, Saiseikai Central Hospital, Tokyo
108, Institute of Clinical Research, National Saitama Hospital,
Saitama 351, Department of Internal Medicine, Shizuoka Red Cross
Hospital, Shizuoka 420, Department of Internal Medicine, School of
Medicine, Keio University, Tokyo 160, Japan
APStracts 3:0123G, 1996.
Topical application of ethanol to the gastrointestinal mucosa induced
vasodilation. Using an in vivo microscopy technique, we studied the
effect of topical ethanol on the submucosal microvessels that control
mucosal blood flow in the rat stomach, and identified vasoactive
substances and receptors that mediate the ethanol vasoaction. 1 to
20% topical ethanol dilated submucosal arterioles dose-dependently,
but did not change venular diameters. An inhibitor of alcohol
dehydrogenase, 1 mM 4-methylpyrazole, did not alter the ethanol
vasoaction. Ethanol-induced arteriolar dilation was eliminated by
adenosine deaminase, but other vasodilator inhibitors, such as
atropine, pyrilamine, indomethacin, human CGRP-(8-37) and L-NAME did
not prevent it. Ethanol-induced arteriolar dilation was inhibited by
an adenosine A2-receptor antagonist, but not by an A1-receptor
antagonist, while an A2-agonist, but not an A1-agonist, dose
-dependently dilated arterioles. Exogenous adenosine, 10-5 to 10-3 M,
dilated arterioles to a similar extent as ethanol. This response was
inhibited by an A2-antagonist. We conclude that non-metabolized
ethanol increases gastric mucosal blood flow via A2-receptors in
submucosal arterioles.
Received 2 January 1996; accepted in final form 23 May 1996.
APS Manuscript Number G5-6.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 June 96