Renin inhibition improves pressure natriuresis in essential hypertension.

Abstract

Pressure natriuresis (PN), i.e., a rise in renal sodium excretion in response to a higher BP, is involved in long-term BP regulation. PN is blunted in essential hypertension, but the mechanism is unknown. This study assessed the role of the renin-angiotensin-aldosterone system (RAAS) in PN in eight essential hypertensive men from the individual correlations between spontaneous fluctuations in BP and time corresponding changes in sodium excretion (collected at 2- and 4-h intervals for 48 h), during strict sodium balance, without treatment, and during renin inhibition (remikiren, 600 mg oral compound). Without treatment, daily values for mean arterial pressure were 109.5 +/- 1.9 and 107 +/- 1.9 mmHg, for urinary sodium excretion were 37.2 +/- 2.8 and 42.0 +/- 2.8 mmol/24 h, and for plasma renin activity were 2.34 +/- 0.48 and 2.23 +/- 0.44 nmol/L per h, respectively, for two consecutive days. During remikiren treatment, mean arterial pressure was 101.9 +/- 1.7 and 100.8 +/- 1. 7 mmHg (P: < 0.05, versus baseline). Urinary sodium excretion was 39. 3 +/- 3.7 and 45.2 +/- 5.3 mmol/24 h (not significant versus baseline), and plasma renin activity was 0.79 +/- 0.11 and 0.82 +/- 0.13 nmol/L per h (P: < 0.05 versus baseline). During remikiren treatment, BP correlated positively with sodium excretion in all patients but in only three of eight patients without treatment. The slope of the regression equation was steeper during remikiren treatment in seven of eight patients. Thus, the relationship between BP and natriuresis was more readily apparent during RAAS blockade, suggesting that RAAS activity blunts PN in hypertensive patients. Improved PN may contribute to the hypotensive effect of RAAS blockade and to maintenance of sodium balance at a lower BP level without volume expansion.