Fifteen years ago, Bartter et al1 described a syndrome of secondary hyperaldosteronism, characterized by juxtaglomerular hyperplasia and, paradoxically, by the absence of the expected rise in blood pressure (BP). The clinical and biochemical facets of this syndrome have since been delineated, but its mechanism remains obscure, even though the dimness of the pathophysiologic horizon has been lit up at intervals by a succession of colorful hypotheses. Unfortunately, like falling stars they shone briefly, only to fade away.
Bartter attributed his newly discovered syndrome to insensitivity of the arterial wall to the pressor effects of angiotensin. The resultant hemodynamic disturbance is sensed by the kidney as contracted blood volume, to which the kidney responds by oversecreting renin. Excess renin in turn stimulates aldosterone secretion with consequent potassium loss and metabolic alkalosis. As a result of chronic overactivity, the juxtaglomerular apparatus hypertrophies. Yet, because the blood vessels are unable to constrict