Renal prostaglandins and the control of renin release.
This study examines the hypothesis that the renal prostaglandins function as essential mediators in stimulus-secretion coupling for one or more of the basic receptor mechanisms in the control of renin release. Changes in plasma renin activity (PRA) were evaluated in response to suprarenal aortic constriction before and after indomethacin administration in conscious dogs with either a single denervated nonfiltering kidney or with intact filtering kidneys. Suprarenal aortic constriction was adjusted to reduce renal perfusion pressure below the autoregulatory range in both groups of dogs. Inhibition of cyclooxygenase with indomethacin significantly decreased urinary prostaglandin E2 (PGE2) excretion, but indomethacin failed to block or attenuate the increase in PRA in response to a decrease in renal perfusion pressure in either group of dogs. These results fail to support the hypothesis that the renal prostaglandins function as essential mediators of the intrarenal receptor mechanisms for renin release which are activated by a decrease in renal perfusion pressure below the autoregulatory range.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003714:Denervation; D015232:Dinoprostone; D004285:Dogs; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D011311:Pressoreceptors / Q000502:physiology; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000652:urine; D012079:Renal Circulation / Q000187:drug effects; D012083:Renin / Q000097:blood*
D011453:Prostaglandins; D011458:Prostaglandins E; D012083:Renin; D015232:Dinoprostone; D007213:Indomethacin