Adenosine enhances nitric oxide production by vascular endothelial
cells.
Li, Jian-Ming, Richard A. Fenton, Bruce S. Cutler, and James G.
Dobson, Jr.
Division of Vascular Surgery and Department of Physiology,
University of Massachusetts Medical School, Worcester, MA 01655
APStracts 2:0215C, 1995.
Adenosine, per se, is a potent vasodilator of vascular smooth muscle.
Endothelial cells modulate vascular tone via the release of nitric
oxide (NO), which also elicits vasodilation. This study was
undertaken to determine whether adenosine could directly stimulate
endothelial cells to enhance NO production which could subsequently
reduce vascular tone. NO production was evaluated in porcine carotid
artery endothelial (PCAEC) and human saphenous vein endothelial cells
(HSVEC) seeded on multi-well plates, grown to confluence, and treated
with adenosine for one hour. The bathing medium was collected and the
NO production was determined as reflected by the formaton of NO2- and
NO3-. Nitric oxide production by PCAEC was significantly increased by
adenosine in a dose-dependent manner, whereas there was only an
insignificant tendency for an increase by HSVEC. The addition of the
NO synthase competitive inhibitor, NMMA, or the adenosine receptor
antagonist, theophylline, prevented the increase in NO production by
adenosine. The results suggest that adenosine stimulates, by a
receptor mediated mechanism, the production of nitric oxide by
arterial, but not by venous, endothelial cells.
Received 3 April 1995; accepted in final form 22 May 1995.
APS Manuscript Number C185-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 May 1995.