Abstract
There are many published studies on hypertension in the black population from both South Africa and elsewhere on the continent. However, much information stems from studies on so-called ‘African-Americans’. While there may be some valid comparisons, it is important, both for genetic and environmental reasons, to he circumspect in the interpretation of studies of black hypertension performed in populations not resident in Africa. The purpose of this paper then is to briefly review some of the pathogenetic mechanisms and clinical effects of both benign and malignant hypertension with special reference to work done in our department. Some of the work is still ongoing, hut allows for reasonable postulates and from which stem logical avenues for future investigations. The Republic of South Africa is largely a temperate region with a population of about 40 million (75% blacks, 17% whites, 6% mixed race and 2% Asian). About 40% of the population are ‘semi-rural’ and the rest urban or peri-urban. Hypertension occurs in about 28% of the black population (HB) and about 18% in whites (HW).’-’ Because of Westernization of rural areas, the previously quoted prevalence of ‘rural’ hypertension of 10% is now fast approaching urban levels4 Hypertension is more severe in the black population, occurs at a younger age and more frequently causes end-organ fa i l~re .~ It is associated with a low renin status in over two-thirds of patients and the response to a pressure naturesis is subobtimal. As a group HB demonstrate the metabolic insulin resistance syndrome in which obesity, abnormal glucose tolerance and hypertension develops in the absence of overt dyslipidaemia. However, thiazide diuretics do produce dyslipidaemia but less so than in HW.6,7
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