Acute local effects of angiotensin II on the intestinal vasculature.

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Abstract
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.