Urinary and plasma endothelin 1 in essential hypertension and in hypertension secondary to renoparenchymal disease.

An alteration in renal metabolism of endothelin may contribute to hypertension in the SHR and it has been shown that the excretion rate of endothelin is reduced in patients with essential hypertension. We measured plasma and urinary endothelin 1 (ET-1) in 20 untreated essential hypertensives with normal renal function, in eight normotensive healthy subjects, and in 13 hypertensive patients with primary renoparenchymal disease. Plasma ET-1 was higher (P < 0.01) in essential hypertensives (median 1.69, interquartile range 1.2-3.3 pg/ml) than in normal subjects (0.84, 0.37-1.10 pg/ml) but significantly less (P < 0.01) than in hypertensives with renoparenchymal disease (3.57, 1.45-9.52 pg/ml). ET-1 levels slightly correlated with diastolic pressure in essential hypertensives (r = 0.43, P < 0.05) and tended to be correlated with systolic pressure in hypertensives with renal disease (r = 0.47, P = 0.08). ET-1 excretion in essential hypertensives (137, 99-154 ng/24 h) and in normal subjects (120, 62-150 ng/24 h) was significantly lower than in renal hypertensives (191, 123-241 ng/24 h). The ET clearance/GFR ratio (ClET/GFR) was markedly reduced (30%, 21-67%) in essential hypertensives and substantially raised in renal hypertensives (164%, 86-314%) in comparison with normal subjects (83%, 35-94%). Since the ClET/GFR ratio should be 100% if all filtered ET-1 is excreted, the data indicate that ET-1 is synthesized at a reduced rate and/or broken down at an enhanced rate by the kidney in essential hypertension and confirm that there is a high ET-1 generation rate in remnant nephrons in hypertension secondary to renal disease.