Hypertension is a prevalent condition in the United States and is growing. This

Question

Hypertension is a prevalent condition in the United States and is growing. This pathology inordinately affects the African American population with 43% of black males and 45.7% of black females diagnosed with this pathology. This population also develop high blood pressure at a lower age than other ethnic groups.   One of the dominant theories as to the cause of this racial disparity is a defect in oxidative stress in African Americans. In 500 words or less (with references), propose a cellular mechanism through which this happens and discuss possible gene targets that would be different in African Americans. (Links to an external site.)Links to an external site.

Explanation / Answer

Hypertension in African American population has vicious course to induce glomerular damage, oxidative stress, inflammation, endothelial damage, vascular disease, chronic kidney disease and worsening blood pressure.
Increased prevalence of salt sensitivity & reduced plasma renin levels are evident in hypertensive African Americans. Consumption of a high-salt diet results in hypertension and early onset of renal injury and dysfunction. This is associated with reduced plasma renin activity and angiotensinogen (ATG) concentrations, but accompanied by paradoxical elevations of renal tissue angiotensin (Ag) , tissue Ag receptor 1 (AT1) receptor expression and urinary ATG excretion as well as oxidative stress. Activation of NAD(P)H oxidase in the kidney and cardiovascular tissues inhibits Nrf2 expression, (master regulator of genes encoding many antioxidant and cytoprotective enzymes). African Americans - homozygous for the ACE polymorphism will experience a more rapid reduction in blood pressure following ACE inhibition than those who are heterozygous. Similarly, ATG promoter region variants in this group influences the blood pressure response to an Angiotensin converting enzyme inhibitor (ACEI), but not to a calcium channel blocker. Recent mapping studies have demonstrated genetic variation in the regions of MYH9 and APOL 1 on chromosome 22.

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