ANGIOTENSIN-II SUPPRESSION IS A MAJOR FACTOR PERMITTING EXCRETION OF AN ACUTE SODIUM LOAD IN HUMANS

We examined the role of circulating angiotensin II (ANG II) in the exc retion 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 b asal values (6.6 +/- 1.6 pmol/l), only 7 +/- 8 mmol of Na+ was excrete d 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 ofANG II is one of the major fa ctors permitting the acute increase in Na+ excretion after an intraven ous Na+ load. ANG II has direct actions on Na+ excretion in addition t o its effects on aldosterone.