title: Salt sensitivity: concept and pathogenesis.
abstract: Almost two decades ago, the existence of a subset of essential hypertensive patients, who were sensitive (according to the increase in blood pressure levels) to the intake of a diet with a high salt content, was described. These patients are characterized by an increase in blood pressure and in body weight when switched from a low to a high sodium intake. The increase in body weight is due to the incapacity of the kidneys to excrete the whole intake of sodium until renal perfusion pressure (mean blood pressure) attains a level that is able to restore pressure-natriuresis relationship to values that enable the kidney to excrete the salt ingested or administered intravenously. Salt sensitivity does not seem to depend on the existence of an intrinsic renal defect to handle sodium, but on the existence of subtle abnormalities in the regulation of the sympathetic nervous system, the renin-angiotensin system or endothelial function. It is also relevant that organ damage secondary to arterial hypertension, has been shown in animal models and in hypertensive humans sensitive to a high salt intake to be significantly higher when compared with that of salt-resistant animals or humans. Interestingly, in humans, salt sensitivity has been shown to correlate with microalbuminuria, an important predictor of cardiovascular morbidity and mortality, which correlates with most of the cardiovascular risk factors commonly associated with arterial hypertension. One of these factors is insulin resistance, that usually accompanies high blood pressure in overweight and obese hypertensives. Insulin resistance and hyperinsulinism are present in a significant percentage of hypertensive patients developing cardiovascular symptoms or death. For these reasons, therapy of arterial hypertension must be directed, not only to facilitate the lowering of BP level, but also, to halt the mechanisms underlying the increase in BP, when salt intake is increased. Furthermore, therapy must preferably improve the diminished insulin sensitivity present in salt-sensitive subjects that contribute independently to increased cardiovascular risk.
authors.affiliation: Department of Endocrinology, Hospital Ramón y Cajal, Madrid, Spain.
authors.forename: O
authors.initials: O
authors.lastname: González-Albarrán
authors.forename: L M
authors.initials: LM
authors.lastname: Ruilope
authors.forename: E
authors.initials: E
authors.lastname: Villa
authors.forename: R
authors.initials: R
authors.lastname: García Robles
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000139:chemically induced*; D007333:Insulin Resistance; D012982:Sodium, Dietary / Q000494:pharmacology*
chemical_list: D012982:Sodium, Dietary