The pathogenesis of chronic renovascular hypertension.

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Abstract
This review presents an analysis of the data bearing on the possible primary pathogenic mechanisms in renovascular hypertension. This analysis of the many factors which influence arterial pressure emphasizes that renovascular hypertension is multifactorial in nature. However, in most patients with renovascular hypertension the renin-angiotensin system appears to be a primary pathogenic mechanism; repair of the renal lesion or removal of the involved kidney frequently leads to a decrease in PRA [plasma renin activity] to normal and to a cure of the hypertension. In contrast, in several of the hypertensive animal models evidence is lacking to show hat the renin-angiotensin system is involved in the maintenance of chronic renal hypertension; instead, there is new evidence that another renal pressor mechanism is involved. Antihypertensive factors such as prostaglandins and the renomedullary neutral lipid appear to be involved but it is unclear as to their specific role in the causation of renal hypertension. Evidence is lacking to support the hypothesis of whole body autoregulation in renovascular hypertension. When there is increased activity of the renin-angiotensin system in renovascular hypertension, as in man, both the sympathetic and central nervous systems conceivably could be involved. There is evidence for altered vascular reactivity in arterial tissue of animals with renal hypertension.