Angiotensin II suppression is a major factor permitting excretion of an acute sodium load in humans

Abstract

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.