Literature DB >> 28174181

Cardiovascular benefits associated with higher dietary K+ vs. lower dietary Na+: evidence from population and mechanistic studies.

Alicia A McDonough1, Luciana C Veiras2, Claire A Guevara2, Donna L Ralph2.   

Abstract

The World Health Organization ranks hypertension the leading global risk factor for disease, specifically, cardiovascular disease. Blood pressure (BP) is higher in Westernized populations consuming Na+-rich processed foods than in isolated societies consuming K+-rich natural foods. Evidence suggests that lowering dietary Na+ is particularly beneficial in hypertensive individuals who consume a high-Na+ diet. Nonetheless, numerous population studies demonstrate a relationship between higher dietary K+, estimated from urinary excretion or dietary recall, and lower BP, regardless of Na+ intake. Interventional studies with K+ supplementation suggest that it provides a direct benefit; K+ may also be a marker for other beneficial components of a "natural" diet. Recent studies in rodent models indicate mechanisms for the K+ benefit: the distal tubule Na+-Cl- cotransporter (NCC) controls Na+ delivery downstream to the collecting duct, where Na+ reabsorbed by epithelial Na+ channels drives K+ secretion and excretion through K+ channels in the same region. High dietary K+ provokes a decrease in NCC activity to drive more K+ secretion (and Na+ excretion, analogous to the actions of a thiazide diuretic) whether Na+ intake is high or low; low dietary K+ provokes an increase in NCC activity and Na+ retention, also independent of dietary Na+ Together, the findings suggest that public health efforts directed toward increasing consumption of K+-rich natural foods would reduce BP and, thus, cardiovascular and kidney disease.
Copyright © 2017 the American Physiological Society.

Entities:  

Keywords:  ENaC; NCC; dietary potassium; dietary sodium; hypertension

Mesh:

Substances:

Year:  2017        PMID: 28174181      PMCID: PMC5406991          DOI: 10.1152/ajpendo.00453.2016

Source DB:  PubMed          Journal:  Am J Physiol Endocrinol Metab        ISSN: 0193-1849            Impact factor:   4.310


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