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  • Title: Vasopressin, angiotensin II and renal responses during water immersion in hydrated humans.
    Author: Hammerum MS, Bie P, Pump B, Johansen LB, Christensen NJ, Norsk P.
    Journal: J Physiol; 1998 Aug 15; 511 ( Pt 1)(Pt 1):323-30. PubMed ID: 9679185.
    Abstract:
    1. The hypothesis was tested that in hydrated humans the release of arginine vasopressin and angiotensin II is suppressed by water immersion (WI) and that this is a mechanism of the immersion-induced diuresis and natriuresis. Seven male subjects on controlled sodium (65-75 mmol per 24 h for 4 days) and water intake were studied. 2. Plasma vasopressin 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 water output (CH2O) from -0.4 +/- 0.2 to 4.4 +/- 0.7 ml min-1 (P < 0.05). Subsequently, CH2O returned to the level of control, whereas plasma vasopressin remained suppressed. Plasma osmolality gradually increased 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 decreased from 27.1 +/- 5.3 to 4.3 +/- 0.7 pg ml-1 (P < 0.05), and the intraindividual 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 CH2O and sodium excretion. Therefore, vasopressin could constitute a mediator of CH2O and angiotensin II of the natriuresis of WI. The subsequent return of CH2O to the level of control is, however, also caused by other factors.
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