There is ample reason to believe that, in man, reduced arterial flow to one kidney may result in hypertension. This is evidenced by many reports of long-term reversion to normotension after nephrectomy,1-12 and by some more recently reported short-term results after plastic surgical procedures upon stenotic renal arteries.13-15 The underlying mechanism whereby hypertension is brought about in these situations, however, remains unknown.
In the period immediately following Butler's initial report of restoration of normotension after removal of a diseased kidney,16 many nephrectomies were performed, without benefit to the patients in most instances.17-19 The best results achieved in any of the larger series of cases disclosed that only 30% of the patients had improved. In the past decade further procedures have been devised to evaluate whether or not a morbid kidney is responsible for the hypertension present. It is believed by the authors that (1) proper utilization