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.
aDepartment of Kinesiology and Applied Physiology
bDepartment of Biological Sciences, University of Delaware, Newark, Delaware
cThe John B. Pierce Laboratory
dDepartment of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut
eDepartment of Behavioral Health and Nutrition, University of Delaware, Newark, Delaware
fDivision of Nephrology, Department of Medicine, Nephrology Research and Training Center, Center for Free Radical Biology, University of Alabama at Birmingham
gDepartment of Medicine, Veterans Affairs Medical Center, Birmingham, Alabama, USA
*Both senior authors contributed equally.
Correspondence to David G. Edwards, PhD and William B. Farquhar, PhD, Department of Kinesiology and Applied Physiology, 219 McDowell Hall, 25 North College Avenue, Newark, DE 19716, USA. Tel: +1 302 831 8006; fax: +1 302 831 3693; e-mail: firstname.lastname@example.org@udel.edu
Abbreviations: BP, blood pressure; CVD, cardiovascular disease; EDD, endothelium-dependent dilation; EID, endothelium-independent dilation; FMD, flow-mediated dilation; MAP, mean arterial blood pressure
Received 30 May, 2012
Revised 1 October, 2012
Accepted 8 November, 2012