Role of arginine vasopressin in the regulation of extracellular fluid volume.

Abstract

The Henry-Gauer hypothesis postulates that changes in left atrial pressure induce changes in the release of arginine vasopressin (AVP), which subsequently modulates the renal output of fluid. Results of the past decades indicate that this hypothesis is too simplistic in explaining the complexity of extracellular fluid volume (ECFV) regulation in humans. Factors controlling renal sodium excretion are the primary modulators of ECFV. AVP is probably important in the related adjustments of renal water excretion whereby changes in plasma sodium concentration induce changes in plasma osmolality and, subsequently, in release of AVP. Evidence has accrued that changes in arterial variables, e.g., arterial pulse pressure, induce changes in the release of AVP during acute changes in central blood volume. Thus, arterial baroreflex regulation of AVP release might constitute one of several pathways of ECFV regulation. Recent results from the D2-Spacelab mission on ECFV regulation are surprising. Following an isotonic saline infusion, renal sodium and fluid output were lower than expected from results of simulation experiments, and venous plasma NE and renin higher. Since plasma AVP was low, high levels of this variable cannot constitute an explanation for the attenuated renal output of fluid during flight. Thus, the currently used models (in particular head-down bed rest) for simulating microgravity should be critically reevaluated. In addition, the relationship between central cardiovascular variables, endocrine mediators, and renal function during microgravity should be a focus of future research.