Humoral and mechanical factors modulating neural input to the renal vasculature.
The velocity and magnitude of neurally elicited renal vasoconstrictions decrease with reduction of renal arterial pressure. We investigated the relative roles of humoral and mechanical factors in this decrease. Cats were anesthetized with chloralose. Renal arterial pressure was controlled with an aortic cuff. Vasoconstrictions were elicited by electrical stimulation of the renal nerves until renal vascular resistance stabilized. Renal blood flow autoregulation was maintained during stimulation. Competitive blockade of angiotensin II did not affect the decrease in renal vascular responsiveness to neural input at reduced renal arterial pressure. A mathematical model suggested that a major portion of the decrease in the velocity of vasoconstrictions was a mechanical consequence of autoregulatory vasodilation. However, the model was only able to account for the experimental findings after the blockade of prostaglandin synthesis, and this blockade significantly increased the velocity of vasoconstrictions at renal arterial pressures of 75 Torr or below. These results suggested that prostaglandins as well as mechanical factors played a role in the autoregulatory decrease in responsiveness to sympathetic input.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D002415:Cats; D004558:Electric Stimulation; D005260:Female; D006706:Homeostasis; D007668:Kidney / Q000098:blood supply* / Q000294:innervation; D008297:Male; D008433:Mathematics; D008954:Models, Biological; D011453:Prostaglandins / Q000494:pharmacology; D012039:Regional Blood Flow; D012077:Renal Artery; D014661:Vasoconstriction; D014666:Vasomotor System / Q000502:physiology*
D011453:Prostaglandins; D000804:Angiotensin II