Published online before print February 25, 2008, doi: 10.1161/HYPERTENSIONAHA.107.109652
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(Hypertension. 2008;51:823.)
© 2008 American Heart Association, Inc.
Editorial Commentaries |
Salt Sensitivity
It Is Not Always in the Genes
From the Division of Nephrology, Department of Medicine, Department of Physiology & Biophysics, and Nephrology Research and Training Center, University of Alabama at Birmingham, and the Department of Veterans Affairs Medical Center, Birmingham.
Correspondence to Paul W. Sanders, MD, Division of Nephrology/Department of Medicine, 642 Lyons-Harrison Research Building, 1530 Third Avenue, South, University of Alabama at Birmingham, Birmingham, AL 35294-0007. E-mail psanders@uab.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Although increases in dietary NaCl (referred to as salt in this article) intake expand extracellular fluid volume and elevate mean arterial pressure (MAP) even in healthy subjects, the magnitude of the response varies with some individuals demonstrating remarkable resistance to the hypertensive effects of salt intake despite ingestion of very high doses.1 Salt sensitivity therefore refers to the propensity for changes in salt intake to produce meaningful increases in mean arterial pressure (MAP). The endless debate regarding whether the amount of salt ingested affected blood pressure sufficiently to alter life span was effectively curtailed by the Trials of Hypertension Prevention studies, which showed that dietary salt reduction decreased the long-term risk of cardiovascular events by 25% in patients who had prehypertension, confirming an important effect of salt intake on the cardiovascular system.2 In addition, the landmark work of Weinberger and colleagues provided convincing evidence that normotensive subjects who demonstrated salt sensitivity had a subsequent cumulative mortality that rivaled that of hypertensive patients.3
How salt intake alters cardiovascular function remains uncertain but may be related in part to changes in arterial compliance, a known marker of cardiovascular morbidity and mortality. Gates et al4 demonstrated in a double-blind placebo-controlled crossover experiment that reduction in salt intake in patients with untreated systolic hypertension lowered systolic blood pressure and increased carotid arterial compliance. In that study, the decrease in systolic blood pressure correlated inversely with change in arterial compliance. In rats, an increase in dietary salt intake increased intravascular production of transforming growth factor
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Hypertension 2008 51: 928-932.