Renal prostaglandins and the control of renin release

Ronald H. Freeman, James O. Davis, John R. Dietz, Daniel Villarreal, Andrea A. Seymour, Stephen F. Echtenkamp

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

This study examines tbe 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 Indometfaacin administration in conscious dogs with either a single denervated nonflltering 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 cydooxygenaae with indomethacin significantly decreased urinary prostoglandin E, (PGE,) 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 tbe intrarenal receptor mechanisms for renin release whkh are activated by a decrease in renal perfusion pressure below tbe autoregulatory range.

Original languageEnglish (US)
Pages (from-to)106-112
Number of pages7
JournalHypertension
Volume4
Issue number3
DOIs
StatePublished - May 1982
Externally publishedYes

Keywords

  • Aortic constriction
  • Beta-adrenergic mechanism conscious dogs
  • Excretion
  • Macula densa
  • Nonflltering kidney
  • Renal baroreceptor mechanism
  • Urinary PGE

ASJC Scopus subject areas

  • Internal Medicine

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