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Am J Physiol Renal Physiol 297: F237-F243, 2009. First published April 1, 2009; doi:10.1152/ajprenal.00027.2009
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REVIEW

Vascular consequences of dietary salt intake

Paul W. Sanders

Division of Nephrology, Department of Medicine, and Department of Physiology and Biophysics, University of Alabama at Birmingham, and Department of Veterans Affairs Medical Center, Birmingham, Alabama

Submitted 18 January 2009 ; accepted in final form 26 March 2009

ABSTRACT

Animal and human studies support an untoward effect of excess dietary NaCl (salt) intake on cardiovascular and renal function and life span. Recent work has promoted the concept that the endothelium, in particular, reacts to changes in dietary salt intake through a complex series of events that are independent of blood pressure and the renin-angiotensin-aldosterone axis. The cellular signaling events culminate in the intravascular production of transforming growth factor-β (TGF-β) and nitric oxide in response to increased salt intake. Plasticity of the endothelium is integral in the vascular remodeling consequences associated with excess salt intake, because nitric oxide serves as a negative regulator of TGF-β production. Impairment of nitric oxide production, such as occurs with endothelial dysfunction in a variety of disease states, results in unopposed excess vascular TGF-β production, which promotes reduced vascular compliance and augmented peripheral arterial constriction and hypertension. Persistent alterations in vascular function promote the increase in cardiovascular events and reductions in renal function that reduce life span during increased salt intake.

transforming growth factor-β; nitric oxide; vascular remodeling; arterial compliance


Address for reprint requests and other correspondence: P. W. Sanders, Div. of Nephrology/Dept. of Medicine, 642 Lyons-Harrison Research Bldg., 1530 Third Ave. South, Univ. of Alabama at Birmingham, Birmingham, AL 35294-0007 (e-mail: psanders{at}uab.edu)






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