An alternative hypothesis to the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension

. 2016 Nov ; 90 (5) : 965-973. [epub] 20160818

Jazyk angličtina Země Spojené státy americké Médium print-electronic

Typ dokumentu časopisecké články, přehledy, Research Support, N.I.H., Extramural, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/pmid27546606

Grantová podpora
M01 RR000079 NCRR NIH HHS - United States
R01 HL064230 NHLBI NIH HHS - United States

Odkazy

PubMed 27546606
PubMed Central PMC5065753
DOI 10.1016/j.kint.2016.05.032
PII: S0085-2538(16)30310-6
Knihovny.cz E-zdroje

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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