Prostaglandins are overproduced by the kidneys and mediate hyperreninemia in Bartter's syndrome.

In summary, the cardinal features of the syndrome of renal juxtaglomerular hyperplasia include overproduction of plasma renin activity, elevation of plasma angiotensin II concentration, elevation of aldosterone secretion and of plasma aldosterone concentration, hypokalemic alkalosis, and a resistance of arterioles to the pressor action of angiotensin II and norepinephrine. In the present studies, elevation of urinary PGE2 but not of PGF2alpha has been demonstrated. Inhibition of prostaglandin synthetase with indomethacin or ibuprofen has been shown to decrease plasma renin activity, and plasma aldosterone concentration and secretion rate, leading to a positive potassium balance and restoration of normal plasma potassium. The inhibitors decreased and glomerular filtration rate, and induced sodium retention. The results indicate that overproduction of PGE by the kidneys is a cardinal feature, but not necessary the primary one, in the pathogenesis of this syndrome.