AJP - Heart and Circulatory Physiology, Vol 257, Issue 6 1966-H1970, Copyright © 1989 by American Physiological Society

ARTICLES

Endothelial impairment inhibits prostaglandin and EDRF-mediated arteriolar dilation in vivo

A. Koller, E. J. Messina, M. S. Wolin and G. Kaley
Department of Physiology, New York Medical College, Valhalla 10595.

The role of endothelium in the vasodilation of third order arterioles of cremaster muscle to a variety of vasoactive agents was investigated in pentobarbital-anesthetized rats. Changes in diameter to topical administration of agents were measured with image shearing, before and after mercury light/sodium fluorescein (light/dye) treatment of a 50- to 100-microns segment of the arteriole under study and were recorded with video microscopy. Before light/dye treatment, arachidonic acid (10(-5) M), prostaglandin E2 (5 x 10(-6) M), A23187 (2 x 10(-6) M), acetylcholine (10(-5) M), and adenosine (10(-4) M) elicited dilation between 75 and 106% of basal diameter. After light/dye treatment, dilations to arachidonic acid, A23187, and acetylcholine were completely eliminated; however, the responses to prostaglandin E2 and adenosine were not altered. These results indicate that light/dye treatment interferes with the production of or response to prostaglandins as well as other endothelial mediators, like endothelium-derived relaxing factor (EDRF). In a second series of experiments, bradykinin, in concentrations of 10(-9), 10(-8), and 10(-7) M elicited dose-dependent dilations, which were partially inhibited by indomethacin and completely abolished after additional light/dye treatment. Dilation of arterioles to adenosine was maintained throughout these experiments. These data suggest that vasodilation to bradykinin is mediated partly via prostaglandin production and partly via other endothelium-derived factor(s).

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