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To determine the relationship between endothelin-1 (ET-1), human atrial natriuretic peptide (hANP), plasma-renin activity (PRA) and 24-h urinary excretion of aldosterone (U-Ald) in pregnancy-induced hypertension (PIH).Plasma hANP (pg/ml), ET-1 (pg/ml), PRA (ng/ml per h) and U-Ald (Mg/24 h) were measured and 24 h ambulatory mean arterial pressure (MAP) was monitored in 178 normotensive subjects (NT) and 79 gravidas with PIH at the 8th, 18th, 23rd, 28th, 32nd and 36th weeks.The PIH group had higher MAP than the NT group from the 23rd week (91.64 ± 8.76 versus 83.48 ± 4.36 mmHg, P < 0.01) until the end of the pregnancy. ET-1 levels (pg/ml) in both groups were identical at the beginning of pregnancy and different in the 23rd week [(NT versus PIH) (35.11 ± 17.42 and 40.2 ± 19.51, respectively, P < 0.05)] and the 36th week (37.36 ± 18.07 and 42.7 ± 16.43, P < 0.05). hANP levels (pg/ml) in the NT group decreased insignificantly from the 8th till the 32nd week, then increased to 101.94 ± 17.4 in the 36th (P < 0.001 versus any other week). In the PIH group, hANP increased from 104.8 ± 26.8 pg/ml at the 8th week to 161.3 ± 28.6 pg/ml at the 36th week (P < 0.0001). hANP correlated with MAP in the NT group (r = 0.252, P < 0.0005) but not the PIH group. U-Ald in the NT group increased from 23.52 ± 6.83 μg/24 h at the 8th week to 54.07 ± 19.62 μg/24 h at the 36th week (P < 0.0001) and in the PIH group it increased from 27.90 ± 11.6 to 53.66 ± 20.4 μg/24 h (P < 0.0001). In the PIH group, PRA was lower compared with the NT group from the 8th (2.99 ± 1.26 versus 4.10 ± 1.82 ng/ml per h, P < 0.05) until the 36th week (3.34 ± 2.16 versus 4.46 ± 2.13 ng/ml perh). In the forced multiple regression analysis model with hANP as a dependent variable, a value of P < 0.003 was found with PRA, U-Ald and MAP, which indicates an interaction between the two vasoactive and homeostatic systems: the renin-angiotensin-aldosterone system and hANP.In PIH, elevated hANP might be important as a counterbalance to the presence of the active vasopressors and sodium retention. By inhibiting renin release, enhancing the transcapillary fluid migration and with its action as vasodilator, it acts as a corrective factor of the imbalance between the contracted circulating fluid volume and the vasoconstricted vascular bed.