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      Differences in hypertension between blacks and whites: an overview

      research-article
      , MB ChB, FCP, MMed
      Cardiovascular Journal of Africa
      Clinics Cardive Publishing

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          Summary

          Hypertension is more prevalent and severe in urban black populations compared to whites, and is associated with a greater degree of target-organ damage for any given blood pressure level. In general, compared to whites, blacks respond well to diuretics and calcium channel blockers and less well to β-blockers and ACE inhibitors. The exact mechanisms that contribute to differences in blood pressure between blacks and whites are still not fully understood, given the multi-factorial aetiology of essential hypertension. Various lines of evidence suggest black patients are more salt sensitive than whites, which is due to a tendency to retain sodium in the kidney. Inherent differences in ionic transport mechanisms, the renal epithelial sodium channel, the renin-angiotensin-aldosterone system and vasoactive substances may be a partial explanation, but analysis is compounded by disparate socio-economic conditions between blacks and whites. At present, there is no complete explanation for these differences and further research is required.

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          Most cited references100

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          The kidney, hypertension, and obesity.

          This paper provides a personal perspective of the role of abnormal renal-pressure natriuresis in the pathogenesis of hypertension. Direct support for a major role of renal-pressure natriuresis in long-term control of arterial pressure and sodium balance comes from studies demonstrating that (1) pressure natriuresis is impaired in all forms of chronic hypertension and (2) prevention of pressure natriuresis from operating, by servo-control of renal perfusion pressure, also prevents the maintenance of sodium balance hypertension. Although the precise mechanisms of impaired pressure natriuresis in essential hypertension have remained elusive, recent evidence suggests that obesity and overweight may play a major role. Obesity increases renal sodium reabsorption and impairs pressure natriuresis by activation of the renin-angiotensin and sympathetic nervous systems and by altered intrarenal physical forces. Chronic obesity also causes marked structural changes in the kidneys that eventually lead to a loss of nephron function, further increases in arterial pressure, and severe renal injury in some cases. Although there are many unanswered questions about the mechanisms of obesity hypertension and renal disease, this is one of the most promising areas for future research, especially in view of the growing, worldwide "epidemic" of obesity.
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            Genetic decreases in atrial natriuretic peptide and salt-sensitive hypertension.

            To determine if defects in the atrial natriuretic peptide (ANP) system can cause hypertension, mice were generated with a disruption of the proANP gene. Homozygous mutants had no circulating or atrial ANP, and their blood pressures were elevated by 8 to 23 millimeters of mercury when they were fed standard (0.5 percent sodium chloride) and intermediate (2 percent sodium chloride) salt diets. On standard salt diets, heterozygotes had normal amounts of circulating ANP and normal blood pressures. However, on high (8 percent sodium chloride) salt diets they were hypertensive, with blood pressures elevated by 27 millimeters of mercury. These results demonstrate that genetically reduced production of ANP can lead to salt-sensitive hypertension.
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              Endothelins: molecular biology, biochemistry, pharmacology, physiology, and pathophysiology.

                Author and article information

                Contributors
                Journal
                Cardiovasc J Afr
                Cardiovasc J Afr
                TBC
                Cardiovascular Journal of Africa
                Clinics Cardive Publishing
                1995-1892
                1680-0745
                Jul-Aug 2007
                : 18
                : 4
                : 241-247
                Affiliations
                Division of Hypertension, Department of Medicine, Groote Schuur Hospital and University of Cape Town
                Division of Hypertension, Department of Medicine, Groote Schuur Hospital and University of Cape Town
                Division of Hypertension, Department of Medicine, Groote Schuur Hospital and University of Cape Town
                Article
                4170224
                17940670
                9d4d8d61-0f7a-424b-913c-27e181844965
                Copyright © 2010 Clinics Cardive Publishing

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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