The pivotal role of renal vasodysfunction in salt sensitivity and the initiation of 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_____%2F18%3A00489811" target="_blank" >RIV/67985823:_____/18:00489811 - isvavai.cz</a>
Result on the web
<a href="http://dx.doi.org/10.1097/MNH.0000000000000394" target="_blank" >http://dx.doi.org/10.1097/MNH.0000000000000394</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1097/MNH.0000000000000394" target="_blank" >10.1097/MNH.0000000000000394</a>
Alternative languages
Result language
angličtina
Original language name
The pivotal role of renal vasodysfunction in salt sensitivity and the initiation of salt-induced hypertension
Original language description
For decades, it has been widely accepted that initiation of salt-induced hypertension involves a type of kidney dysfunction (natriuretic handicap), which causes salt-sensitive subjects to initially excrete less of a sodium load than normal subjects and undergo abnormal increases in cardiac output, and therefore blood pressure. Here we discuss emerging views that renal vasodysfunction, not natriuretic dysfunction (subnormal sodium excretion), is usually a critical factor initiating salt-induced hypertension. Serious logical issues have been raised with arguments supporting historical views that natriuretic dysfunction initiates hypertension in response to increased salt intake. Most salt-sensitive humans do not have a 'natriuretic handicap' causing them to excrete a sodium load more slowly and retain more of it than salt-resistant normal subjects. Mounting evidence indicates that in most salt-sensitive subjects, renal vasodysfunction, defined as impaired renal vasodilation and abnormally increased renal vascular resistance in response to increased salt intake, in the absence of greater sodium retention than in saltloaded normal subjects, is involved in initiation of salt-induced hypertension. To advance discovery, prevention, and treatment of primary abnormalities causing salt-induced hypertension, greater research emphasis should be placed on identifying mechanisms mediating subnormal renal vasodilation and abnormally increased renal vascular resistance in response to high-salt diets.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30101 - Human genetics
Result continuities
Project
—
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2018
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Current Opinion in Nephrology and Hypertension
ISSN
1062-4821
e-ISSN
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Volume of the periodical
27
Issue of the periodical within the volume
2
Country of publishing house
US - UNITED STATES
Number of pages
10
Pages from-to
83-92
UT code for WoS article
000429661000005
EID of the result in the Scopus database
2-s2.0-85042447776