1. Nifedipine (20 mg) was given by mouth to seven patients with moderate essential hypertension receiving a low, normal or high sodium intake. The drug produced an important hypotensive effect. Normal sodium intake enhanced the hypotensive action of the drug compared with that during the low and high sodium regimens. Blood pressure remained significantly lower 3 h after drug ingestion.2. Increases in heart rate and plasma renin activity under all conditions reflected enhanced adrenergic activity.3. A short-term natriuresis followed nifedipine ingestion in spite of increased aldosterone excretion during the low sodium diet and a decrease in urinary kallikrein during the low and high sodium diets. 4. Nifedipine increased urinary volume only during the high sodium intake. 5. Apart from vasodilatation, nifedipine induces important changes in neurogenic, renal and adrenal mechanisms that regulate blood pressure homoeostasis. Different conditions of sodium balance modulate most of these effects.

In a single-dose crossover study Captopril (SQ 14225), 1 mg/kg body weight, and Nifedipine (Bay a 1040) 20 mg were administered orally to 12 hospitalized patients with essential hypertension (Stage 1 or 2, W.H.O.). Both drugs significantly reduced blood pressure, but each dose acted differently: the mean maximum arterial pressure reduction was faster and greater with Nifedipine than with Captopril: -23 +/- 2% at 37 +/- 15 min and -17 +/- 1% at 86 +/- 25 min, respectively. Captopril inhibited angiotensin II and aldosterone production, but did not accelerate heart rate or stimulate vasopressin release. Nifedipine stimulated vasopressin release and increased heart rate, but the renin angiotensin aldosterone system was not significantly affected. The blood pressure reduction was related to the initial level of activation of the renin angiotensin system only for Captopril. The blood pressure reduction induced by one drug was not related to that produced by the other in the same patient.

Plasma concentrations and urinary excretion rate of vasopressin (VP) were examined in ten cases of severe hypertension before and during short-term treatment by Captopril (SQ 14225). Before Captopril, plasma and urinary VP were high (respectively 5.24 pmol/l and 68 pmol/day) and positively correlated to plasma renin activity (PRA) and plasma aldosterone (PA). The decline in blood pressure (mean -15%) after Captopril was correlated not only to initial PRA and PA values, but also to plasma (r = 0.89; P less than 0.001) and urinary (r = 0.78; P less than 0.01) VP values. The initial dose of Captopril (1 mg/kg) induced a rapid decrease in blood pressure whereas plasma VP did not rise and aldosterone decreased. At the eighth day of Captopril treatment (mean daily dose 6 +/- 1.5 mg/kg) the drop in blood pressure (-12%) and in aldosterone persisted together with a significant reduction in plasma (1.18 pmol/l; P less than 0.01) and urinary (25 pmol/day; P less than 0.01) VP. It is suggested that these sustained simultaneous reductions in the rates of secretion of vasopressin and aldosterone are both elements of the antihypertensive effect of Captopril.

Summarvof severe forms of hvDertension. The reduction of vasopressin during captopril treatment could be an additional mechanism underlying the antihypertensive effect of that drug. Moreover, from it appears that antihypertensive drugs have 1. Plasma vasopressin was estimated in 20 normotensive9 46 moderate hype*ensive and l4 sodium diet. values for plasma vasopressin (PVP) after over-(UVP) were respectively 1.82 f 0.23 pmol/l and Severe hype*ensive patients under the comparison between nifedipine and captopril, 2* In moderate hypertensive patients different effects on vasopressin release. night dehydration and 24 urinary vasopressin

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