An alternative hypothesis to the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, přehledy, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
M01 RR000079
NCRR NIH HHS - United States
R01 HL064230
NHLBI NIH HHS - United States
PubMed
27546606
PubMed Central
PMC5065753
DOI
10.1016/j.kint.2016.05.032
PII: S0085-2538(16)30310-6
Knihovny.cz E-zdroje
- Klíčová slova
- blood pressure, hypertension, kidney, salt, salt-resistance, salt-sensitivity, sodium, sodium chloride,
- MeSH
- hypertenze etiologie MeSH
- krevní objem účinky léků MeSH
- kuchyňská sůl škodlivé účinky metabolismus farmakologie MeSH
- lidé MeSH
- sodík metabolismus MeSH
- studie případů a kontrol MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Research Support, N.I.H., Extramural MeSH
- Názvy látek
- kuchyňská sůl MeSH
- sodík MeSH
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.
Department of Laboratory Medicine University of California San Francisco California USA
Department of Medicine University of California San Francisco California USA
Department of Physiology Wayne State University Detroit Michigan USA
Institute of Physiology Czech Academy of Sciences Prague Czech Republic
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