Renin inhibition improves pressure natriuresis in essential hypertension

Pressure natriuresis (PN), i.e., a rise in renal sodium excretion in respon se 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 spontan eous 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 com pound). 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 da ys. During remikiren treatment, mean arterial pressure was 101.9 +/- 1.7 an d 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 baselin e), and plasma renin activity was 0.79 +/- 0.11 and 0.82 +/- 0.13 nmol/L pe r h (P < 0.05 versus baseline). During remikiren treatment, BP correlated p ositively with sodium excretion in all patients but in only three of eight patients without treatment. The slope of the regression equation was steepe r during remikiren treatment in seven of eight patients. Thus, the relation ship between BP and natriuresis was more readily apparent during RAAS block ade, suggesting that RAAS activity blunts PN in hypertensive patients. Impr oved PN may contribute to the hypotensive effect of RAAS blockade and to ma intenance of sodium balance at a lower BP level without volume expansion.