AJP - Heart and Circulatory Physiology, Vol 253, Issue 6 1573-H1580, Copyright © 1987 by American Physiological Society
Endogenous prostaglandins selectively mask large arteriole constriction to angiotensin II
J. T. Fleming, P. D. Harris and I. G. Joshua
Department of Physiology and Biophysics, School of Medicine, University of Louisville, Kentucky 40292.
Television microscopy was used to observe the responses of in vivo
arterioles and venules of the rat cremaster muscle to the topical
application of angiotensin II (10(-8) and 10(-6) M). Neither the first-
(A1) or second-order arterioles (A2) nor the first- (V1) or second-order
venules (V2) constricted significantly to angiotensin II. However, after
the inhibition of local prostaglandin synthesis with either mefenamic acid
or indomethacin, both A1 and A2, but not the venules, gave a significant
constrictor response to angiotensin II (10(-6) M). Arterioles and venules,
which were preconstricted with norepinephrine, dilated to their initial
baseline diameters after angiotensin II (10(-6) M), a response not observed
when the microvessels were pretreated with either an angiotensin antagonist
or a prostaglandin synthesis inhibitor. These observations indicate that
endogenous prostaglandins exert a significant dilator influence on the
larger arterioles, that this dilator influence appears to oppose the
constrictor effect of angiotensin II, and that angiotensin II acts on
specific receptors to induce synthesis and/or release of dilator
prostaglandins in large arterioles. However, prostaglandins cannot account
for the absence of a venular constriction to angiotensin.
