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AJP - Renal Physiology, Vol 266, Issue 1 89-F93, Copyright © 1994 by American Physiological Society
ARTICLES |
D. R. Singer, N. D. Markandu, J. J. Morton, M. A. Miller, G. A. Sagnella and G. A. MacGregor
Department of Physiological Medicine, St. George's Hospital Medical School, London, United Kingdom.
We examined the role of circulating angiotensin II (ANG II) in the excretion of an acute Na+ load in eight healthy subjects given 2 liters 0.9% saline in a placebo-controlled crossover study. On the control day, plasma ANG II decreased to 40-60% of basal values and 35 +/- 9 (SE) mmol of Na+ was excreted in the 5 h after the start of saline infusion. When ANG II was infused to maintain plasma ANG II levels at around basal values (6.6 +/- 1.6 pmol/l), only 7 +/- 8 mmol of Na+ was excreted in the same period (P < 0.05). In a previous similar study in which the fall in aldosterone was prevented by infusion of aldosterone, 16 +/- 16 mmol of Na+ was excreted vs. 36 +/- 16 mmol on the control day in comparable 5-h periods. Suppression of ANG II is one of the major factors permitting the acute increase in Na+ excretion after an intravenous Na+ load. ANG II has direct actions on Na+ excretion in addition to its effects on aldosterone.
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