Enhanced antinatriuresis in response to angiotensin II in essential hypertension

Abstract

Angiotensin II regulates sodium homeostasis by modulating aldosterone secretion, renal vascular response, and tubular sodium reabsorption. We hypothesized that the antinatriuretic response to angiotensin II is enhanced in human essential hypertension. We therefore studied 48 white men with essential hypertension (defined by ambulatory blood pressure measurement) and 72 normotensive white control persons, and measured mean arterial pressure, sodium excretion, renal plasma flow, glomerular filtration rate, and aldosterone secretion in response to angiotensin II infusion (0.5 and 3.0 ng/kg/min). Hypertensive 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 flow (−151.5 ± 73.9 mL/min v −112.6 ± 68.0 mL/min in controls, P < .01) when 3.0 ng/kg/min angiotensin II was infused. The increase of glomerular filtration rate and serum aldosterone concentration 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, the 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 concentration. Our data suggest a hyperresponsiveness to angiotensin II in essential hypertension that could lead to increased sodium retention.