Role of peripheral angiotensin in salt appetite of the sodium-deplete rat

Abstract

Lines of evidence indicate that the importance of peripherally derived angiotensin II as a stimulus for salt appetite in rats has been underestimated. First, a series of observations is consistent with the idea that peripherally derived angiotensin acts at circumventricular organs of the brain to stimulate salt appetite following sodium depletion. Second, recent experiments show that depletion-induced salt appetite is abolished by the i.v. infusion of converting-enzyme inhibitor (captopril) at a dose that totally prevents the formation of angiotensin II within the peripheral circulation. This same dose of converting-enzyme inhibitor does not penetrate the blood-brain barrier to affect the actions of centrally derived angiotensin. These findings suggest that angiotensin II of peripheral origin is critical for the expression of salt appetite following extracellular fluid depletions. Together, these two lines of evidence suggest that the role of circulating angiotensin II in the stimulation of salt appetite in the rat should be re-examined.