An alternative hypothesis to the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F16%3A00465060" target="_blank" >RIV/67985823:_____/16:00465060 - isvavai.cz</a>
Result on the web
<a href="http://dx.doi.org/10.1016/j.kint.2016.05.032" target="_blank" >http://dx.doi.org/10.1016/j.kint.2016.05.032</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.kint.2016.05.032" target="_blank" >10.1016/j.kint.2016.05.032</a>
Alternative languages
Result language
angličtina
Original language name
An alternative hypothesis to the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension
Original language description
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.
Czech name
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Czech description
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Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
FA - Cardiovascular diseases including cardio-surgery
OECD FORD branch
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Result continuities
Project
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Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2016
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Kidney International
ISSN
0085-2538
e-ISSN
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Volume of the periodical
90
Issue of the periodical within the volume
5
Country of publishing house
US - UNITED STATES
Number of pages
9
Pages from-to
965-973
UT code for WoS article
000386547100012
EID of the result in the Scopus database
2-s2.0-84994087060