Enhanced antinatriuresis in response to angiotensin II in essential hypertension

Angiotensin II regulates sodium homeostasis by modulating aldosterone secre tion, renal vascular response, and tubular sodium reabsorption. We hypothes ized that the antinatriuretic response to angiotensin II is enhanced in hum an essential hypertension. We therefore studied 48 white men with essential hypertension (defined by ambulatory blood pressure measurement) and 72 nor motensive white control persons, and measured mean arterial pressure, sodiu m excretion, renal plasma now, glomerular filtration rate, and aldosterone secretion in response to angiotensin II infusion (0.5 and 3.0 ng/kg/min). H ypertensive subjects exhibited a greater increase of mean arterial pressure (16.7 +/- 8.2 mm Hg v 13.4 +/- 7.1 mm Hg in normotensives, P < .05) and a greater decrease of renal plasma now (-151.5 +/- 73.9 mL/min v -112.6 +/- 6 8.0 mL/min in controls, P < .01) when 3.0 ng/kg/min angiotensin II was infu sed. The increase of glomerular filtration rate and serum aldosterone conce ntration was similar in both groups. Sodium excretion in response to 3.0 ng /kg/min angiotensin II was diminished in both groups (P < .01). However, th e decrease in sodium excretion was more pronounced in hypertensives than in normotensives (-0.18 +/- 0.2 mmol/min v -0.09 +/- 0.2 mmol/min, P < .05), even if baseline mean arterial pressure and body mass index were taken into account (P < .05). We conclude that increased sodium retention in response to angiotensin II exists in subjects with essential hypertension, which is unrelated to changes in glomerular filtration rate and aldosterone concent ration. Our data suggest a hyperresponsiveness to angiotensin II in essenti al hypertension that could lead to increased sodium retention. Am J Hyperte ns 2000;13:986-993 (C) 2000 American Journal of Hypertension, Ltd.