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Department of Aviation Medicine, The Heart Centre, The National University Hospital, DK-2100 Copenhagen; Department of Medical Physiology, University of Copenhagen, DK-2200 Copenhagen; Department of Clinical Physiology and Nuclear Medicine, Glostrup University Hospital, DK-2600 Glostrup; Department of Internal Medicine and Endocrinology, Herlev University Hospital, DK-2730 Herlev; Department of Cardiology, Gentofte University Hospital, DK-2900 Hellerup; and Department of Physiology and Pharmacology, University of Southern Denmark, DK-5000 Odense, Denmark
The hypothesis was tested that
suppression of generation of ANG II is one of the mechanisms of the
water immersion (WI)-induced natriuresis in humans. In one protocol,
eight healthy young males were subjected to 3 h of 1)
WI (WI + placebo), 2) WI combined with ANG II infusion
of 0.5 ng · kg
1 · min1 (WI + ANG II-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 ANG II by
the lithium clearance method (CLi) and were on an
additional fourth study day subjected to infusion of ANG II at a rate
of 1.5 ng · kg1 · min1
(WI + ANG II-high). During WI + placebo, plasma concentration of ANG II decreased from 16 ± 2 to 8 ± 1 pg/ml
(P < 0.05) and renal sodium excretion increased from
104 ± 15 to 294 ± 27 µmol/min (P < 0.05). During WI + ANG II-low, plasma ANG II was not suppressed by
WI, and the natriuresis was blunted by 52 ± 13%
(P < 0.05). During WI + ANG II-low and WI + ANG II-high, an increase in CLi was prevented that was
otherwise observed during WI, and fractional distal reabsorption of
sodium was facilitated. In conclusion, maintaining plasma concentration
of ANG II unchanged at the level of control attenuates the natriuresis
of WI considerably in humans. Therefore, suppression of generation of
ANG II is an important mechanism of the natriuresis of WI in humans.
Furthermore, infusion of ANG II during WI prevents an otherwise induced
increase in CLi and facilitates the fractional distal
reabsorption of sodium, probably via an effect on aldosterone release.
sodium excretion; tubular function
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