Salt appetite: its neuroendocrine basis

Abstract

Based on the early work of Richter (1936), showing that the adrenalectomized rat kept itself alive by drinking hypertonic NaCl solutions, Epstein and Stellar (1955) demonstrated that that salt appetite was innate, not dependent on learning. A series of later papers by Epstein and his students made clear that in addition to the adrenal steroid, aldosterone, salt appetite depended upon the action of angiotensin II in the brain. Blocking either hormone in the brain reduced depletion-induced salt appetite in half; blocking both eliminated it. Two salt depletions enhanced depletion-induced salt appetite by nearly a factor of two even when the rats never had a chance to drink salt in the first depletion. With multiple depletions, need-free salt intake also increased when the rats were sodium replete, producing an chronic, elevated salt appetite. Strikingly, female rats drink almost twice as much as males and become more enhanced by prior depletions. The neural circuitry involved in the synergy of angiotensin and aldosterone is becoming clearer with lesions of the amygdala that reduce aldosterone's effects and lesions of the anterior wall of the third ventricle that reduce angiotensin's effects. The significance of salt appetite in nature, in body fluid homeostasis, and as a model system of the brain mechanisms of ingestive behavior is discussed.