Renin inhibition improves pressure natriuresis in essential hypertension

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