Hypertension, Vol 6, 13-19, Copyright © 1984 by American Heart Association
RA Nyhof, TG Rascoe and HJ Granger
The vasotoxic properties of angiotensin II (AII) on vascular endothelial
cells have been implicated in the increased extravasation of proteins and
water observed in certain forms of chronic arterial hypertension. Since
microvascular permeability in the small intestine is increased in
one-kidney, one clip hypertension, we tested the hypothesis that AII
decreases the permselectivity of intestinal microvessels to plasma
proteins. The acute intestinal vascular effects of AII were studied by
locally infusing AII into isolated canine jejunal segments. A measure of
vascular permeability in control and infused segments was obtained by
estimating the osmotic reflection coefficient as 1-lymph/plasma protein
concentration ratio when the ratio reached a plateau at high lymph flows.
Lymph flows were increased by raising the venous pressure from a control of
5 to 30-35 mm Hg in 5 mm Hg steps. Resting control blood and lymph flows
were reduced by AII, but these flows were not different at the higher
venous pressures due to the apparent blunting of the venous-arteriolar
response by AII. The estimated osmotic reflection coefficient of 0.85 for
the control animals was less than that obtained in the infused segments
(0.93). This effect was substantiated by electrophoretic separation of
protein fractions. Thus, AII per se does not cause an acute increase in
intestinal vascular permeability, and may, in fact reduce it.
ARTICLES
Acute local effects of angiotensin II on the intestinal vasculature
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