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

DuPont, Jennifer J.a; Greaney, Jody L.a,b; Wenner, Megan M.c,d; Lennon-Edwards, Shannon L.a,e; Sanders, Paul W.f,g; Farquhar, William B.a,b,*; Edwards, David G.a,b,*

doi: 10.1097/HJH.0b013e32835c6ca8
ORIGINAL PAPERS: Endothelium

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: dge@udel.eduorwbf@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

© 2013 Lippincott Williams & Wilkins, Inc.