Title of article :
Pathophysiology of Salt-Sensitive Hypertension.
Author/Authors :
J. G. Douglas، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1995
Pages :
1
From page :
4
To page :
4
Abstract :
The higher incidence, severity, morbidity, and mortality of hypertension in African-Americans has been attributed to genetic and environmental factors. Employing heritability estimates genetics have been assessed as accounting for 30-60% of the variation in blood pressure while shared environmental factors account for <10% in families. There is ample evidence that environmental factors including access to health care, socioeconomic status, stress, diet, obesity and other risk factors account for some of the ethnic/racial differences in blood pressure prevalence worldwide. Genetically determined sensitivity to high salt intake or other inciting agents also contributes to excess hypertension in African-Americans. The heritability of Na sensitivity of blood pressure regulation has been documented in twin vs. siblings analyses and in haptoglobin phenotyping. Several factors has been implicated in the pathophysiology of hypertension in African-Americans. Fifty to 70% percents of the African-American population have an enhanced capacity for renal salt reabsorption versus 27 percent in the hypertensive White population. A similar discrepancy has been observed between normotensive relatives of African-American and White hypertensives. Renal salt retention leads to an expanded plasma volume with inhibition of the renin angiotensin aldosterone system. Other characteristics of “salt-sensitive” subjects include older age, brisk natriuretic response to an acute sodium load, lower PRA, but steeper PRA/ALDO relationships and enhanced efficacy of diuretic antihypertensive agents as compared to ACE inhibitors and β-blockers.
Keywords :
salt-sensitivity , African-Americans , Race/Ethnicity~ Genetics
Journal title :
American Journal of Hypertension
Serial Year :
1995
Journal title :
American Journal of Hypertension
Record number :
646050
Link To Document :
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