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Sodium Appetite During Captopril Blockade of Endogenous Angiotensin Formation

  • Karen Moe
  • Alan N. Epstein
Part of the NATO ASI Series book series (NSSA, volume 105)

Abstract

Activation of the renin-angiotensin-aldosterone system during sodium deficiency is directly or indirectly responsible for many compensatory physiological responses which act to conserve both sodium and water1. Moreover, there is a large and increasing body of evidence for a role of angiotensin (ANG) in salt appetite, the behavioral partner to these conservation mechanisms. For example, it is well-established that administration of ANG can arouse a salt appetite in sodium-replete rats2,3. However, in natural situations, ANG probably acts in conjunction with aldosterone. Epstein and colleagues have recently shown that when the two hormones are administered together, at very low doses they act synergistically to produce the appetite4. Thus, concurrent elevation of the two hormones, as in sodium deficiency, may be an important mechanism by which the appetite is aroused.

Keywords

Peripheral Administration Sodium Depletion Depletion Period Sodium Deficiency Salt Appetite 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1986

Authors and Affiliations

  • Karen Moe
    • 1
  • Alan N. Epstein
    • 1
  1. 1.Department of Biology and Institute of Neurological SciencesUniversity of PennsylvaniaPhiladelphiaUSA

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