Evidence for a renomedullary vasodepressor hormone

Colleen Thomas, Robyn Woods, Roger G Evans, Daine Alcorn, Irene Christy, Warwick Anderson

Research output: Contribution to journalReview ArticleResearchpeer-review

31 Citations (Scopus)


1. Recent physiological experiments have established that increasing the perfusion pressure of the kidney causes the release of a vasodepressor substance from the renal medulla. 2. The substance is not a platelet activating factor, a prostaglandin or nitric oxide and the vasodepressor response to increased renal perfusion pressure is not due simply to inhibition of renin release. 3. The mechanisms by which the renomedullary vasodepressor substance lowers arterial pressure remain to be determined. Sympathoinhibition may account for part of the response, but the hypotension still occurs in autonomic ganglion blocked animals. 4. The source of the substance appears to be the renomedullary interstitial cells, though the control of the production and release of the substance remain to be determined. 5. The substance may be a lipid but it is yet to be fully isolated and identified. 6. The threshold for release of the substance appears to be close to normal resting arterial blood pressure. 7. Despite strong evidence that the renal medulla releases a vasodepressor hormone in response to increased renal perfusion pressure, much is still to be determined regarding the physiology of this hormone and its involvement in the aetiology of hypertension.

Original languageEnglish
Pages (from-to)777-785
Number of pages9
JournalClinical and Experimental Pharmacology and Physiology
Issue number9
Publication statusPublished - 1 Jan 1996
Externally publishedYes


  • Blood pressure
  • Hypertension
  • Kidney
  • Medullipin
  • Renal blood flow
  • Renal medulla

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