Mechanisms of renal hypertension and renal contribution to primary hypertension

Abstract

Investigators in hypertension have extensively evaluated the mechanisms of hypertension as first described by Goldblatt in his classic clipped kidney models. Although renovascular hypertension appears to affect only 2–4% of the population referred for diagnostic studies of hypertension, our understanding of renovascular hypertension has broadened from the interaction of the renin-angiotensin system to the inclusion of the activation of the sympathetic nervous system and locally mediated prostaglandins. This increased understanding of renal mediated abnormalities has also led to the implication that abnormalities in renal function may be the main abnormality in primary hypertension. It has been demonstrated that early, mildly hypertensive patients may have an increase in total body volume. This elevated volume may lead to autoregulation which persistently elevates vascular resistance. The renal abnormality leading to an abnormal pressure-volume relationship may be related to a decrease in renal plasma flow mediated by an increase in arteriolar resistance. This increase in vascular tone has been ascribed to an increase in sympathetic nerve activity, an increase in renin and/or an increase in catechols and angiotensin II. It has also been suggested that ischemic nephrons in a microvascular model akin to the classic Goldblatt two kidney-one clip model may be the pathologic abnormality underlying primary hypertension. These concepts of renovascular hypertension and primary renal dysfunction are reviewed in this conference.