Genetics of salt-sensitive hypertension

Curr Hypertens Rep. 2011 Feb;13(1):55-66. doi: 10.1007/s11906-010-0167-6.

Abstract

The assessment of salt sensitivity of blood pressure is difficult because of the lack of universal consensus on definition. Regardless of the variability in the definition of salt sensitivity, increased salt intake, independent of the actual level of blood pressure, is also a risk factor for cardiovascular morbidity and mortality and kidney disease. A modest reduction in salt intake results in an immediate decrease in blood pressure, with long-term beneficial consequences. However, some have suggested that dietary sodium restriction may not be beneficial to everyone. Thus, there is a need to distinguish salt-sensitive from salt-resistant individuals, but it has been difficult to do so with phenotypic studies. Therefore, there is a need to determine the genes that are involved in salt sensitivity. This review focuses on genes associated with salt sensitivity, with emphasis on the variants associated with salt sensitivity in humans that are not due to monogenic causes. Special emphasis is given to gene variants associated with salt sensitivity whose protein products interfere with cell function and increase blood pressure in transgenic mice.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Blood Pressure / drug effects
  • Blood Pressure / genetics
  • Cardiovascular Diseases / embryology
  • Cardiovascular Diseases / genetics
  • Cardiovascular Diseases / pathology
  • Gene Expression
  • Humans
  • Hypertension / chemically induced
  • Hypertension / epidemiology
  • Hypertension / genetics*
  • Kidney Diseases / epidemiology
  • Nitric Oxide Synthase / drug effects
  • Nitric Oxide Synthase / genetics
  • Renin-Angiotensin System / drug effects*
  • Risk Factors
  • Sodium, Dietary / administration & dosage*
  • Sodium, Dietary / metabolism
  • Sympathetic Nervous System / drug effects
  • United States / epidemiology

Substances

  • Sodium, Dietary
  • Nitric Oxide Synthase