Salt sensitivity: a review with a focus on non-Hispanic blacks and Hispanics

Abstract

The purpose of this review is to summarize the available information regarding salt sensitivity particularly as it relates to non-Hispanic blacks and Hispanics and to clarify possible etiologies, especially those that might shed light on potential treatment options. In non-Hispanic blacks, there is evidence that endothelial dysfunction, reduced potassium intake, decreased urinary kallikrein excretion, upregulation of sodium channel activity, dysfunction in atrial natriuretic peptide (ANP) production, and APOL1 gene nephropathy risk variants may cause or contribute to salt sensitivity. Supported treatment avenues include diets high in potassium and soybean protein, the components of which stimulate nitric oxide production. Racial heterogeneity complicates the study of salt sensitivity in Hispanic populations. Caribbean Hispanics, who have a higher proportion of African ancestry, may respond to commonly prescribed anti-hypertensive agents in a way that is characteristic of non-Hispanic black hypertensives. The low-renin hypertensive phenotype commonly seen in non-Hispanic blacks has been linked to salt sensitivity and may indicate an increased risk for salt sensitivity in a portion of the Hispanic population. In conclusion, increased morbidity and mortality associated with salt sensitivity mandates further studies evaluating the efficacy of tailored dietary and pharmacologic treatment in non-Hispanic blacks and determining the prevalence of low renin hypertension and salt sensitivity within the various subgroups of Hispanic Americans.

Copyright © 2013 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.

Figures

Figure 1

Survival curves for salt sensitive and salt resistant subjects. Kaplan-Meier survival curves for normotensive salt-resistant subjects (N+R), normotensive salt-sensitive subjects (N+S), hypertensive salt-resistant subjects (H+R), and hypertensive salt-sensitive subjects (N+S) over the follow-up period. As noted, only the N+R group had an increased survival. Adapted from Weinberger et al.

Figure 2

Flow diagram detailing the role of kallikrein in promoting diuresis. Kallikrein secretion, triggered by excess sodium in the connecting tubule, generates renal kinins which act on the brady-kinin receptor 2 (BK B2 R) to promote diuresis.