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2017 ; 28
(5
): 1362-1369
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Novel Paradigms of Salt and Hypertension
#MMPMID28220030
Feng W
; Dell'Italia LJ
; Sanders PW
J Am Soc Nephrol
2017[May]; 28
(5
): 1362-1369
PMID28220030
show ga
Salt resistance/sensitivity refers specifically to the effect of dietary sodium
chloride (salt) intake on BP. Increased dietary salt intake promotes an early and
uniform expansion of extracellular fluid volume and increased cardiac output. To
compensate for these hemodynamic changes and maintain constant BP in salt
resistance, renal and peripheral vascular resistance falls and is associated with
an increase in production of nitric oxide. In contrast, the decline in peripheral
vascular resistance and the increase in nitric oxide are impaired or absent in
salt sensitivity, promoting an increase in BP in these individuals. Endothelial
dysfunction may pose a particularly significant risk factor in the development of
salt sensitivity and subsequent hypertension. Vulnerable salt-sensitive
populations may have in common underlying endothelial dysfunction due to genetic
or environmental influences. These individuals may be very sensitive to the
hemodynamic stress of increased effective blood volume, setting in motion
untoward molecular and biochemical events that lead to overproduction of TGF-?,
oxidative stress, and limited bioavailable nitric oxide. Finally, chronic
high-salt ingestion produces endothelial dysfunction, even in salt-resistant
subjects. Thus, the complex syndrome of salt sensitivity may be a function of the
endothelium, which is integrally involved in the vascular responses to high salt
intake.
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