High dietary sodium intake impairs endothelium-dependent dilation in healthy salt-resistant humans

Abstract

Background: Excess dietary sodium has been linked to the development of hypertension and other cardiovascular diseases. In humans, the effects of sodium consumption on endothelial function have not been separated from the effects on blood pressure. The present study was designed to determine if dietary sodium intake affected endothelium-dependent dilation (EDD) independently of changes in blood pressure.

Method: Fourteen healthy salt-resistant adults were studied (9M, 5F; age 33 ± 2.4 years) in a controlled feeding study. After a baseline run-in diet, participants were randomized to a 7-day high-sodium (300-350 mmol/day) and 7-day low-sodium (20 mmol/day) diet. Salt resistance, defined as a 5 mmHg or less change in a 24-h mean arterial pressure, was individually assessed while on the low-sodium and high-sodium diets and confirmed in the participants undergoing study (low-sodium: 85 ± 1 mmHg; high-sodium: 85 ± 2 mmHg). EDD was determined in each participant via brachial artery flow-mediated dilation on the last day of each diet.

Results: Sodium excretion increased during the high-sodium diet (P < 0.01). EDD was reduced on the high-sodium diet (low: 10.3 ± 0.9%, high: 7.3 ± 0.7%; P < 0.05). The high-sodium diet significantly suppressed plasma renin activity (PRA), plasma angiotensin II, and aldosterone (P < 0.05).

Conclusion: These data demonstrate that excess salt intake in humans impairs endothelium-dependent dilation independently of changes in blood pressure.

Figure 1

Urinary sodium excretion (Panel A; P < 0.01) and mean arterial pressure (MAP, Panel B; P = 0.87) during the LS (filled bars) and HS (open bars) diets. Renal function curve (Panel C) demonstrating that despite a significant increase in sodium intake/excretion during the HS diet, 24-hour MAP did not change, affirming the salt-resistant phenotype. * P<0.05. LS; low sodium. HS; high sodium.

Figure 2

Plasma renin activity (A), plasma angiotensin II (B), and plasma aldosterone (C). Compared to corresponding values obtained during the LS diet, all were suppressed (P<0.05) during the HS diet. LS; low sodium. HS; high sodium.

Figure 3

Individual (Panel A) and group (Panel B) endothelium-dependent dilation (EDD) responses during the LS and HS diets. EDD was significantly decreased during the HS diet. Endothelium-independent dilation EID (Panel C) did not differ between the LS and HS diets. *P < 0.05. LS; low sodium. HS; high sodium.