Renal hypertension.
Continuing interest in the mechanism of hypertension have produced considerable new information on the underlying pathophysiologic processes involved. Elucidation of the role of renal malperfusion, the renin-angiotensin-aldosterone mechanism, and renal medullary antihypertensive substances continues to clarify our understanding of renal hypertension. Current evidence suggests that angiotensin can produce hypertension by a direct effect on peripheral blood vessels in malignant hypertension and in renin-secreting renal tumors and by an intrarenal mechanism influencing intrarenal distribution of blood flow, and, thereby, sodium resorption in chronic renovascular hypertension. The current diagnostic techniques used to determine the presence of renal atery stenosis and its functional significance are reviewed. Arteriographic evidence of renal artery collaterals and a positive differential venous renin ratio are the two parameters whose usefulness and practicality have been best documented in recent years. The results of surgical procedures reported in the world literature show a 50 per cent rate with a further 30 per cent improvement rate in terms of control of hypertension. When functional significance of stenosis is demonstrated before surgical procedures, cure rates of the order of 80 per cent can be achieved. Recent developments of technique of operating room upon less extensive lesions of the renal artery branch extend the possibilities of surgical benefit which should also be considered in the presence of renal failure of renovascular origin.
D000450:Aldosterone / Q000502:physiology; D000804:Angiotensin II / Q000502:physiology; D006801:Humans; D006977:Hypertension, Renal / Q000175:diagnosis / Q000503:physiopathology / Q000601:surgery; D011379:Prognosis; D012078:Renal Artery Obstruction / Q000175:diagnosis / Q000601:surgery; D012083:Renin / Q000502:physiology
D000804:Angiotensin II; D000450:Aldosterone; D012083:Renin