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Exaggerated salt appetite of spontaneously hypertensive rats is decreased by central angiotensin-converting enzyme blockade

Nature volume 298, pages 846–848 (1982)Cite this article

Abstract

Injection of angiotensin II (AII) into the cerebral ventricles at doses as low as 1 pmol h−1 results in a marked stimulation of salt and water ingestion in the rat1,2. Evidence that AII is produced in the central nervous system independently of the circulating renin–angiotensin system (RAS)3,4 raises the possibility that endogenous brain AII is involved in the physiological regulation of thirst5. The role of brain AII in salt appetite is still unclear6. Here we confirm that the spontaneously hypertensive rat (SHR), believed to have elevated levels of brain AII7, possesses an exaggerated salt appetite compared with its nor-motensive controls. We also show that this exaggerated salt appetite is reduced by chronic central treatment with the angiotensin-converting enzyme inhibitor, captopril, while that of the normotensive controls is unaffected. Our study suggests that a central neuropeptide, probably AII, is involved in the maintenance of the exaggerated salt appetite in this model of hypertension.

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Authors and Affiliations

  1. University of Melbourne, Department of Medicine, Austin Hospital, Heidelberg, Victoria, 3084, Australia

    R. DiNicolantonio, J. S. Hutchinson & F. A. O. Mendelsohn

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  1. R. DiNicolantonio
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  2. J. S. Hutchinson
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  3. F. A. O. Mendelsohn
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DiNicolantonio, R., Hutchinson, J. & Mendelsohn, F. Exaggerated salt appetite of spontaneously hypertensive rats is decreased by central angiotensin-converting enzyme blockade. Nature 298, 846–848 (1982). https://doi.org/10.1038/298846a0

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