Renal Kininase I, Kininase II and Neutral Endopeptidase 24.11 Adtivities in Patients with Essential Hypertension, Primary Aldosteronism and Cushing's Syndrome.

Abstract

To further clarify the role of renal kininases in various hypertensive diseases, daily urinary excretions of total kininase, kininase I, kininase II and neutral endopeptidase 24.11(NEP) were examined in patients with essential hypertension (EHT), primary aldosteronism (PA) and Cushing's syndrome. In this study, a new method for the simultaneous determination of human urinary kininase I, II and NEP activities was employed. Total kininase and NEP levels in EHT (579.7 ±79.3, 358.8±53.4μg/min/day), PA (928.8 ±212.8, 278.5±24.4) and Cushing's syndrome (605.7±25.3, 359.9±78.4) were significantly higher than in normotensives (NT: 261.9±29.6, 151.4±10.2). Kininase I levels in PA (100.1±23.4μg/min/day) and Cushing's syndrome (76.6±12.7), but not in EHT (71.8 ±11.5), were significantly higher than in NT (38.2±4.2). Kininase II was significantly higher than in NT (72.2±10.2), only in Cushing's syndrome (137.9±2.4), and levels in EHT (131.1±22.0) and PA (126.7±23.7) were not. Unexpectedly, these three kininases accounted for 62% of total kininase in PA, and almost 100% of total kininase in EHT, Cushing's syndrome and NT. These findings suggest that: 1) NEP may play a major role in the metabolism of renal kinins in man. 2) NEP in EHT, NEP and kininase I in PA and NEP, and kininase I and II in Cushing's syndrome are increased. 3) An unknown kininase, different from these three kininases, may exist in PA. 4) Enhanced renal kininases may play an important role in disorders of renal water-sodium metabolism and blood pressure in these hypertensive diseases by regulating the metabolism of intrarenal kinins. (Hypertens Res 1993; 16: 253-258)