Journal
KIDNEY INTERNATIONAL
Volume 90, Issue 5, Pages 965-973Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.kint.2016.05.032
Keywords
blood pressure; hypertension; kidney; salt; salt-resistance; salt-sensitivity; sodium; sodium chloride
Categories
Funding
- General Clinical Research Center, Moffitt-Long Hospital, University of California, San Francisco, California
- National Center for Research Resources, U.S. Public Health Service [M0 RR-00079]
- Praemium Academiae award of the Czech Academy of Sciences
- National Institutes of Health/National Heart, Lung, and Blood Institute [RO1-HL64230]
- Antel Foundation
- Maier Family Foundation
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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.
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