Histamine H1 receptor antagonists inhibit autoregulation of renal blood flow in the dog.

Abstract

Histamine H1 and H2 receptors are present in the canine renal circulation. We have examined the effects of H1 and H2 receptor antagonists on autoregulation of renal blood flow in the dog. Renal arterial pressure was reduced in a step-wise fashion to 80 mm Hg by means of an adjustable aortic clamp positioned above the left renal artery. Infusion of H2 antagonists, cimetidine or ranitidine, into the left renal artery at 10(-5) mol/min had no effect on autoregulation of renal blood flow or on the reactive hyperemia that occurred when the aortic constriction was released. By contrast, intrarenal infusion of 10(-5) mol/min chlorpheniramine, an H1 receptor antagonist, reversibly attenuated reactive hyperemia and the ability of the kidney to autoregulate renal blood flow. Similar results were obtained with other, chemically dissimilar H1 antagonists (terfenadine, diphenhydramine, and pyrilamine). The effects of chlorpheniramine on autoregulation of glomerular filtration rate also were evaluated. Before chlorpheniramine was infused (at 10(-5) mol/min), the reduction of renal arterial pressure to 90 mm Hg had no effect on the glomerular filtration rate, whereas, during infusion of the H1 antagonist, the glomerular filtration rate fell significantly when renal arterial pressure was reduced to 90 mm Hg. Infusion of histamine (1 microgram/kg per min) with increasing amounts of cimetidine, chlorpheniramine, diphenhydramine, or pyrilamine resulted in virtually identical dose-dependent decreases in histamine-induced renal vasodilation. However, even with 10(-5) mol/min cimetidine or 10(-5) mol/min chlorpheniramine, diphenhydramine, or pyrilamine, a significant histamine-induced renal vasodilation was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Histamine in the kidneys: what is its role in renal pathophysiology?

“…Autoregulation of renal blood flow is a defensive mechanism that protects the kidney from elevation in arterial pressure and that allows the kidney to maintain a relatively constant GFR (Burke, Pabbidi, Farley, & Roman, 2014). The experimental data are in favour of an active role of at least the extrarenal histamine in regulating GFR, as a possible effector of the renal blood flow autoregulation via H 1 receptors (Banks, Inscho, & Jacobson, 1984). Indeed, after the intrarenal infusion of chlorpheniramine (10−5 mol·min−1) or other H 1 receptor antagonists/inverse agonists, with a variety of chemical structures (terfenadine, diphenhydramine, and mepyramine), attenuated the hyperaemia evoked by aortic clamping.…”

“…Indeed, after the intrarenal infusion of chlorpheniramine (10−5 mol·min−1) or other H 1 receptor antagonists/inverse agonists, with a variety of chemical structures (terfenadine, diphenhydramine, and mepyramine), attenuated the hyperaemia evoked by aortic clamping. Furthermore, a drop in the GFR was measured in parallel (Banks et al, 1984). A similar effect was observed when H 1 receptor antagonists were used to counteract the renal vasodilation induced by histamine infusions (Banks et al, 1978).…”

Structure and Function of Smooth Muscle with Special Reference to Mast Cells

“…Н1 receptors mediate the autoregulation of both renal blood flow and glomerular filtration rate in dogs, whereas in rabbits, both effects are present -Н1-mediated contraction and Н2-mediated relaxation of the renal artery [24][25][26].…”

Modest Pressure Natriuresis and Autoregulation during Water Diuresis in Dogs

“…Both myogenic vascular reaction and vascular autocrine or paracrine reaction are likely responsible for these pre glomerular intrinsic resistance changes [11,77]; the myogenic changes in vessel diameter include the proximal arcuate and interlobu lar arteries in the autoregulatory responses [73][74][75][76].…”