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Am J Physiol Regul Integr Comp Physiol (March 22, 2002). doi:10.1152/ajpregu.00536.2001
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Articles in PresS, published online ahead of print March 22, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00536.2001
Submitted on September 4, 2001
Accepted on March 1, 2002

Angiotensin II attenuates the natriuresis of water immersion in humans

Morten Schou1, Anders Gabrielsen1, Niels E Bruun2, Peter Skott2, Bettina Pump1, Harriet Dige-Petersen3, Erik Frandsen3, Peter Bie4, Jorgen Warberg5, Niels J Christensen6, and Peter Norsk1*

1 Department of Aviation Medicine, National University Hospital of Copenhagen, Copenhagen, Denmark
2 Department of Cardiology, Gentofte University Hospital, Hellerup, Denmark
3 Department of Nuclear Medicine, Glostrup University Hospital, Glostrup, Denmark
4 Department of Physiology and Pharmacology, University of Southern Denmark, Odense, Denmark
5 Department of Physiology, University of Copenhagen, Copenhagen, Denmark
6 Department of Endocrinology, Herlev University Hospital, Herlev, Denmark

* To whom correspondence should be addressed. E-mail: pnorsk{at}rh.dk.

The hypothesis was tested that suppression of generation of angiotensin II (AII) is one of the mechanisms of the water immersion (WI)-induced natriuresis in humans. In one protocol, 8 healthy young males were subjected to 3 hours of 1) water immersion (WI+placebo), 2) water immersion combined with angiotensin II-infusion of 0.5 ng/kg/min (WI+AII-low), and 3) a seated time control (CON). In another almost identical protocol, 7-10 healthy young males were investigated to delineate the tubular site(s) of action of AII by the lithium clearance method (CLi), and were on an additional fourth study day subjected to infusion of AII in a rate of 1.5 ng/kg/min (WI+AII-high). During WI+placebo, plasma concentration of AII decreased from 16±2 to 8±1 pg/ml (P<0.05) and renal sodium excretion increased from 104±15 to 294±27 umol/min (P<0.05). During WI+AII-low, plasma AII was not suppressed by WI and the natriuresis was blunted by 52±13 % (P<0.05). During WI+AII-low and WI+AII-high an increase in CLi was prevented which was otherwise observed during WI and fractional distal reabsorption of sodium was facilitated. In conclusion, maintaining plasma concentration of AII unchanged at the level of control attenuates the natriuresis of WI considerably in humans. Therefore, suppression of generation of AII is an important mechanism of the natriuresis of WI in humans. Furthermore, infusion of AII during WI prevents an otherwise induced increase in CLi and facilitates the fractional distal reabsorption of sodium, probably via an effect on aldosterone release.




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