Effects of camp dependent protein kinase and guanylate cyclase inhibition on intestinal microvascular responses to norepinephrine in chronic portal hypertension. Wu, Zhi-Yong, and Joseph N. Benoit. DEPARTMENT OF PHYSIOLOGY, UNIVERSITY OF SOUTH ALABAMA COLLEGE OF MEDICINE, MOBILE, ALABAMA 36688 AND DEPARTMENT OF PHYSIOLOGY AND BIOPHYSICS, LOUISIANA STATE UNIVERSITY MEDICAL CENTER, SHREVEPORT, LOUISIANA 71130
APStracts 3:0225G, 1996.
The purpose of the present study was to determine whether selective blockade of cAMP or cGMP mediated events modulated norepinephrine responses in intestinal microvessels of normal and portal hypertensive rats. Vascular norepinephrine responses were evaluated before and after inhibition of cAMP dependent kinase with Rp -adenosine-3'-5'-cyclic monophosphothioate (Rp-cAMPs) or guanylate cyclase with Ly-83583. Male Sprague-Dawley rats were divided into two groups: portal hypertension by portal vein stenosis and normal controls. The small intestine was prepared for microcirculatory studies. Arteriolar diameter and erythrocyte velocity were monitored, microvascular flow was calculated from velocity and diameter data. The preparation was challenged with incremental concentrations of norepinephrine before and after addition of Rp-cAMPs (50 [mu]M) or LY-83583 (30 [mu]M). Arteriolar diameter and blood flow were significantly elevated in portal hypertensive rats; norepinephrine responses were significantly depressed. LY-83583 did not alter arteriolar diameter, blood flow or norepinephrine responsiveness in normal or portal hypertensive rats. Rp-cAMPs did not affect arteriolar diameter, blood flow or norepinephrine responsiveness in normal rats. However in portal hypertensive rats, Rp-cAMPs reduced blood flow by nearly equal to 20% (p < 0.05) and completely restored vascular norepinephrine responses to normal. The results indicate that cAMP but not cGMP dependent events are primarily responsible for the loss of microvascular norepinephrine responsiveness in portal hypertensive intestine.

Received 5 September 1995; accepted in final form 22 October
1996.
APS Manuscript Number G391-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996