VASOPRESSIN, ANGIOTENSIN-II AND RENAL RESPONSES DURING WATER IMMERSION IN HYDRATED HUMANS

1. The hypothesis was tested that in hydrated humans the release of ar ginine vasopressin and angiotensin II is suppressed by water immersion (WI) and that this is a mechanism of the immersion-induced diuresis a nd natriuresis. Seven male subjects on controlled sodium (65-75 mmol p er 24 h for 4 days) and water intake were studied. 2. Plasma vasopress in was promptly suppressed by WI, declining from 0.76 + 0.13 to 0.23 /- 0.08 pg ml(-1) (P < 0.05), with a concomitant increase in renal wat er output (C-H2O) from -0.4 +/- 0.2 to 4.4 +/- 0.7 ml min(-1) (P < 0.0 5). Subsequently, C-H2O returned to the level of control, whereas plas ma vasopressin remained suppressed. Plasma osmolality gradually increa sed from 285 +/- 1 to 289 +/- 1 mosmol kg(-1) (P < 0.05). WI caused a 9-fold increase in renal sodium excretion. Plasma angiotensin II decre ased from 27.1 +/- 5.3 to 4.3 +/- 0.7 pg ml(-1) (P < 0.05), and the in traindividual correlation coefficients between sodium excretion rates and angiotensin II concentrations varied between 0.73 and 0.96 (P < 0. 002). 3. The data demonstrate that plasma vasopressin and angiotensin II concentrations decrease during WI in hydrated humans, concomitantly with initial increases in C-H2O and sodium excretion. Therefore, vaso pressin could constitute a mediator of C-H2O and angiotensin II of the natriuresis of WI. The subsequent return of C-H2O to the level of con trol is, however, also caused by other factors.