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Jun 23, 2017Article Details
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Main Article Content
Pathophysiological mechanisms of urbanisation-related hypertension and the sodium pressor response in black Zimbabweans
Abstract
This study examined the role of endothelin (ET), the thromboxane A, (TXA2)-prostacyclin (PGI2) ratio (TXA2/PGI2), plasma renin activity (PRA) and urinary aldosterone excretion (ALDO) in urban hypertensive patients and in the sodium pressor response in normotensives. Twenty-seven urban hypertensive patients and the same number of normotensive controls were studied on baseline diet, after 5 days of sodium restriction and after 5 days of sodium loading. Mean arterial blood pressure, plasma and ET values, PRA, TXA2/PGI2 and ALDO were assessed on each diet.
The results showed that baseline PRA was suppressed in the hypertensive patients; this indicates that urbanisation-related hypertension is of the low renin type. ET levels and TXA2/PGI2 were higher in hypertensive than in normotenisve subjects, suggesting an association between high blood pressure and these factors. Although the baseline PRA in hypertensives was suppressed, urinary ALDO was no different from that in the normotensive controls where PRA was normal. In addition, sodium restriction did not increase PRA in hypertensive subjects while it more than doubled it in the controls. However, ALDO in hypertensive patients increased to levels that were no different from those in the normotensive subjects. Sodium loading increased blood pressure, ET values and TXA2/PGI2 indicating an association between the latter two factors and the sodium pressor response in those with hypertension. ALDO decreased to similar levels on sodium loading in the two groups. This decrease in ALDO was accompanied by suppression of PRA only in normotensive subjects.
In conclusion, the low-renin-activity urban hypertensives we studied had increased baseline ET levels and TXA2/PGI2. The observed pressor response was accompanied by increases in these two factors. This suggests an important role for the two factors in this form of hypertension and the sodium response in normotensives.
