BARORECEPTORS AND HORMONES IN THIRST AND SALT APPETITE

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DESCRIPTION: The present proposal builds upon the investigator's prior investigations of fluid-related afferent signaling and central processing. The proposed research will employ recently developed models in the rat that permit the investigation of interactive hormonal (angiotensin) and the neural (arterial and cardiopulmonary baroreceptor) afferent signals that control hypovolemic thirst and salt appetite. Preliminary experiments demonstrate that decreases and increases in arterial pressure [AP] respectively facilitate and inhibit water drinking induced by intraventricular angiotensin II. Part 1 of the proposal examines modulatory effects of arterial pressure [AP] on the generation of salt appetite following acute sodium depletion. A second series of preliminary experiments demonstrate that rats lacking arterial baroreceptor input to the brain after surgical removal of the relevant nerves (i.e., denervation of the carotid sinus and aortic arch baroreceptors) have impaired salt intakes in two experimental models of sodium depletion-induced salt appetite that rely largely on the actions of ANG II to produce the salt appetite. Part 2 of this proposal extend this line of investigation to the contributions of another set of vascular neural sensors, i.e. cardiopulmonary baroreceptors, to the salt appetite that follows sodium depletion. A recent, third series of studies has implicated the renal nerves in the production of salt appetite following extracellular fluid depletion. Part 3 of this proposal will continue this research to determine if renal afferent or efferent nerves provide the basis for this phenomenon.