MECHANISM FOR CHANGES IN VASOPRESSIN DURING ACUTE EXPOSURE AT 3 ATM ABS AIR

Mechanism for changes in vasopressin during acute exposure at 3 atm ab s air. Am. J. Physiol. 273 (Regulatory Integrative Comp. Physiol. 42): R259-R264, 1997.-Plasma arginine vasopressin (AVP) concentration is r educed in human subjects during prolonged saturation dive exposures of 4 atmospheres absolute (atm abs) and greater. The objectives of the p resent study were to determine if AVP would be reduced in eight male s ubjects during a 1-h exposure of 3 atm abs air and, if so, to determin e the mechanisms responsible for the AVP response. Assessments of tran smural central venous pressure (central venous pressure - esophageal p ressure) and cardiac volume measurements were made to evaluate the pos sible role of cardiopulmonary receptors on the AVP response. Also, pla sma osmolality (P-osmol), venous blood gases, and mean corpuscular vol ume (MCV) were determined to evaluate potential effects of osmorecepto r and other fluid shifts on AVP release. AVP decreased (P < 0.05) by 0 .5 mu U/ml at 3 atm abs, whereas the transmural central venous pressur e and cardiac volume remained unchanged throughout the experimental pe riods. A significant reduction (P < 0.05) in P-osmol (by similar to 3 mosmol/kgH(2)O) was detected at 3 atm abs. Therefore, we conclude that the reduction in P-osmol may cause the reduction in AVP during exposu re to 3 atm abs pressure. The reduction in P-osmol without water intak e requires the postulation of an internal source of water. We propose that the threefold increase (P < 0.01) in venous Po-2 and concomitant decrease (P < 0.05) in venous MCV suggest that the red blood cell may contribute to hypotonicity at 3 atm abs.