Acetylcholine- and flow-induced production and release of nitric
oxide in arterial and venous endothelial cells.
Fukaya, Yukio, and Toshio Ohhashi.
The 1st Department of Physiology, Shinshu University School of
Medicine, 3-1-1 Asahi, Matsumoto 390, Japan
APStracts 2:0313H, 1995.
In order to study flow-mediated responses in a conduit vein, we
investigated the physiological characteristics of endothelium
-dependent acetylcholine (ACh)- and flow-induced relaxations using a
conventional bioassay cascade. Cylindrical segments isolated from
canine common carotid arteries and external jugular veins were
perfused at a constant mean flow rate ranging from 1 to 8 ml/min.
Endothelium-derived nitric oxide activity in perfusion effluent
through the arterial and venous segments was measured by relaxation
of endothelium-denuded arterial and arterial and/or venous rings
precontracted by prostaglandin F2[alpha], respectively. Stimulation
by a flow rate of 8 ml/min on the arterial and venous endothelial
cells produced about 60 % and 20 % of the maximum relaxation in the
arterial and venous rings, respectively. ACh (10-6 and 10-5 M)
perfused through the arterial and venous segments with endothelium
caused dose-related relaxations of the both bioassay rings. The ACh-
and flow-induced relaxation were completely reduced by mechanical
removal of the endothelial cells. Pretreatment with 5 x 10-5 M L
-nitro-arginine methylester (L-NAME) produced a significant reduction
of the ACh- and flow-induced vasodilation. Additional treatment with
10-4 M L-arginine significantly reversed the L-NAME-induced
inhibition of ACh-induced relaxation, but had no effect on flow
-induced relaxation. When the flow rate was increased from 2 to 4
ml/min, the same concentrations of ACh produced larger dose-related
relaxations than those obtained at a flow rate of 2 ml/min.
Pretreatment with 25 U/ml superoxide dismutase caused no significant
effect on the flow-mediated potentiation of ACh-induced relaxation.
These findings suggest that venous endothelial cells of canine large
vein are able to produce and release of nitric oxide by the
stimulation of increased flow or ACh with a significantly lesser
extent compared with the artery, and that ACh-induced vasodilation is
potentiated by an increase of shear stress up to about 4 dynes/cm2
loaded on the endothelial cells.
Received 22 November 1994; accepted in final form 12 July 1995.
APS Manuscript Number H1037-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.