AJP - Renal Physiology, Vol 249, Issue 6 851-F857, Copyright © 1985 by American Physiological Society
Renal vasodilation with ureteral occlusion and prostaglandins: attenuation by histamine H1 antagonists
R. O. Banks and E. D. Jacobson
We evaluated the effects of histamine receptor antagonists on the renal
vasodilatory responses to ureteral occlusion (UO), to the intrarenal
infusion of prostaglandins E2, I2, A2, D2 and E1, and to bradykinin. We
also determined the effects of meclofenamic acid, a cyclooxygenase
inhibitor, on histamine-induced renal vasodilation and the effects of
2-methylhistamine (2-MeH), and H1 agonist, on glomerular filtration rate
(GFR) and renal blood flow (RBF). Experiments were performed on adult
mongrel dogs anesthetized with pentobarbital sodium. RBF was measured with
an electromagnetic flow probe. Neither UO-induced nor prostaglandin- (PG)
induced renal vasodilation was affected by infusion of the histamine H2
receptor antagonist cimetidine into the renal artery at 10(-5) M/min. On
the other hand, renal artery infusion of the H1 receptor antagonist
chlorpheniramine (CP) at 10(-5) M/min blocked UO-induced renal vasodilation
[RBF increased 34 +/- 4% (SE) prior to but only 2 +/- 2% during infusion of
CP) and markedly attenuated PGI2-, PGA2-, and PGE2-induced increases in RBF
(CP inhibited 64 +/- 9% of the PGE2-induced renal vasodilation). CP had
less effect on the renal vasodilation associated with infusion of PGD2 or
PGE1 and had no effect on the vasodilation induced by bradykinin. Infusion
of exogenous histamine (1 micrograms X kg-1 X min-1) into the renal artery
prior to ureteral occlusion resulted in a typical H1 + H2-mediated
vasodilatory response (RBF increased 53 +/- 7%).(ABSTRACT TRUNCATED AT 250
WORDS)
