Novel Paradigms of Salt and Hypertension.
J Am Soc Nephrol
; 28(5): 1362-1369, 2017 May.
Article
en En
| MEDLINE
| ID: mdl-28220030
ABSTRACT
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-ß, 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.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Cloruro de Sodio Dietético
/
Hipertensión
Tipo de estudio:
Risk_factors_studies
Límite:
Animals
/
Humans
Idioma:
En
Revista:
J Am Soc Nephrol
Asunto de la revista:
NEFROLOGIA
Año:
2017
Tipo del documento:
Article