Abstract
This study investigates the influence of salt intake on renin–angiotensin–aldosterone system and clarifies their role to the target organ damage in the treated hypertensive patients. Subjects were 188 treated hypertensive outpatients (96 females and 92 males, mean age 67 ± 11 y). Patients underwent 24-hour home urine collection to measure urinary salt excretion and proteinuria. Clinical blood pressure (BP) and blood chemistry including plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were determined. Left ventricular mass index (LVMI) was also determined by echocardiography. Average BP was 129 ± 16/68 ± 10 mm Hg with the use of 2.0 antihypertensive drugs on average. Urinary salt excretion, PRA, and PAC were 8.1 ± 3.2 g/day, 2.2 ± 2.8 ng/mL/h, and 112 ± 54 pg/mL, respectively. Even in the patients taking angiotensin receptor blocker or angiotensin-converting enzyme inhibitors (n = 146), 15.1% showed low PRA (<0.5 ng/mL/h) levels and salt excretion in these patients with low PRA (9.1 ± 4.2 g/day) did not differ from those with higher PRA levels (8.2 ± 2.6 g/day, NS). There was no correlation between salt excretion and PRA (r = 0.03, NS), while salt excretion showed a significant negative correlation to PAC (r = −0.17, P < .05). Urinary salt excretion was also correlated with proteinuria (r = 0.25, P < .01) and LVMI (r = 0.16, P < .05). In the multivariate analysis, salt excretion contributed to proteinuria (P < .05) or LVMI (P = .11) independent of age, sex, serum creatinine, and BP levels. Results indicate that PRA levels were relatively low and unaffected by salt intake in Japanese patients treated with antihypertensive drugs. Since high salt intake was possibly associated with target organ damages, strict salt reduction should be encouraged.