title: An alternative hypothesis to the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension.
abstract: It is widely held that in response to high salt diets, normal individuals are acutely and chronically resistant to salt-induced hypertension because they rapidly excrete salt and retain little of it so that their blood volume, and therefore blood pressure, does not increase. Conversely, it is also widely held that salt-sensitive individuals develop salt-induced hypertension because of an impaired renal capacity to excrete salt that causes greater salt retention and blood volume expansion than that which occurs in normal salt-resistant individuals. Here we review results of both acute and chronic salt-loading studies that have compared salt-induced changes in sodium retention and blood volume between normal subjects (salt-resistant normotensive control subjects) and salt-sensitive subjects. The results of properly controlled studies strongly support an alternative view: during acute or chronic increases in salt intake, normal salt-resistant subjects undergo substantial salt retention and do not excrete salt more rapidly, retain less sodium, or undergo lesser blood volume expansion than do salt-sensitive subjects. These observations: (i) directly conflict with the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension, and (ii) have implications for contemporary understanding of how various genetic, immunologic, and other factors determine acute and chronic blood pressure responses to high salt diets.
authors.affiliation: Department of Laboratory Medicine, University of California, San Francisco, California, USA. Electronic address: Ted.Kurtz@ucsf.edu.
authors.forename: Theodore W
authors.initials: TW
authors.lastname: Kurtz
authors.affiliation: Department of Physiology, Wayne State University, Detroit, Michigan, USA.
authors.forename: Stephen E
authors.initials: SE
authors.lastname: DiCarlo
authors.affiliation: Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
authors.forename: Michal
authors.initials: M
authors.lastname: Pravenec
authors.affiliation: Department of Medicine, University of California, San Francisco, California, USA.
authors.forename: Olga
authors.initials: O
authors.lastname: Schmidlin
authors.affiliation: Department of Medicine, University of California, San Francisco, California, USA.
authors.forename: Masae
authors.initials: M
authors.lastname: Tanaka
authors.affiliation: Department of Medicine, University of California, San Francisco, California, USA.
authors.forename: R Curtis
authors.initials: RC
authors.lastname: Morris
mesh_terms: D001810:Blood Volume / Q000187:drug effects*; D016022:Case-Control Studies; D006801:Humans; D006973:Hypertension / Q000209:etiology*; D012964:Sodium / Q000378:metabolism; D017673:Sodium Chloride, Dietary / Q000009:adverse effects* / Q000378:metabolism* / Q000494:pharmacology
chemical_list: D017673:Sodium Chloride, Dietary; D012964:Sodium
keywords: blood pressure; hypertension; kidney; salt; salt-resistance; salt-sensitivity; sodium; sodium chloride