Plasma "prorenin"-renin in Bartter's syndrome, cystic fibrosis, and chloride deficiency, and the effect of prostaglandin synthetase inhibition.

In Bartter's syndrome and in other states with ECFV contraction, very high active plasma renin (PRA greater than 78 ng/ml/hr) is associated with an essential absence of prorenin. In patients whose PRA is less than 50 ng/ml/hr, prorenin accumulates significantly. Patients with Bartter's syndrome treated with PG synthetase inhibitors for 1 week respond with a profound drop in renin, together with a rise in prorenin. Thus, in general, highest active renin values coexist with virtually no prorenin, moderately high renins with rising prorenin, and renins "blocked" by PG synthetase inhibitors with highest prorenin levels. Such a reciprocity between prorenin and renin suggests systemic conversion by means of a convertase mechanism apparently susceptible to PG synthetase inhibitors in vivo but not in vitro. It is also possible that these inhibitors suppress in vivo, but not in vitro, renal renin release more than prorenin release, so that the relative level of prorenin increases. This, coupled with decreased conversion to renin, may contribute to the observed elevation of prorenin.