Angiotensin II mediates increased small intestinal fluid absorption with extracellular volume depletion in the rat.

The purpose of this study was to determine if the increase in small intestinal fluid absorption observed after extracellular fluid (ECF) reduction is mediated by angiotensin II (AII). Infusion of AII at doses that increase plasma levels of the hormone within the physiological range stimulates jejunal fluid absorption. In contrast, at pharmacological doses that result in plasma AII levels unlikely to be encountered normally, the hormone inhibits absorption and/or stimulates jejunal secretion. The AII stimulation of jejunal fluid absorption is potentiated by nephrectomy, suggesting that the endogenous levels of AII are related to and have an important role in regulation of the cellular level of its own receptors. Extracellular volume reduction as a result of sodium depletion, nonhypotensive hemorrhage, or water deprivation increases jejunal fluid absorption 30-40% above control values. This increase in jejunal absorption after ECF reduction is not affected by adrenalectomy, but is abolished by nephrectomy, either alone or in combination with adrenalectomy. Captopril, prazosin, and peripheral sympathectomy also abolish the increase in jejunal absorption following ECF depletion. It is suggested that AII is generated after ECF reduction and increases jejunal fluid absorption by facilitating the release of norepinephrine from enteric sympathetic nerves. Thus, AII is a physiologically important mediator of jejunal fluid absorption.