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We studied the effects of infusion of dopamine (4 microgram/kg/min for 120 min) alone or with domperidone infusion (235 microgram/min for 120 min) on aldosterone secretion before and after stimulation by ACTH (0,5 mg i.v.) in normal subjects. We also studied the effects, of pimozide (12 mg p.o.), of domperidone infusion (235 microgram/min for 120 min) before and after stimulation with ACTH (0,5 mg i.v.) on aldosterone secretion in two other sets of normal subjects. The infusion of dopamine does not modify the basal secretion of aldosterone whereas in other trials it caused reduction (P less than 0,05) of blood aldosterone response to ACTH versus controls. Domperidone and pimozide, D2 antagonist, do not modify the aldosterone secretion before and after ACTH stimulation. Furthermore domperidone does not remove inhibition of dopamine on aldosterone response to ACTH. We can exclude an action of central or peripheral D2 dopaminergic receptors in aldosterone secretion in man. Dopamine, which does not cross the blood brain barrier, reduced the blood aldosterone response to ACTH; for those reasons we can hypothesize that receptors D1, stimulated by dopamine modulate aldosterone secretion.

In beef isolated and superfused adrenal glands, the Authors have studied the production of aldosteron and tissue concentration of cAMP during superfusion with angiotensin II alone or preceededby preincubation with indomethacin or verapamil. In such experimental conditions the Authors could evidence that th aldosterone-inductor effect of angiotensin II is not mediated by cAMP but by PGs and Ca++.

The authors studied the blood aldosterone, cortisol and kalium levels, the plasma renin activity and the aldosterone urinary excretion following L-DOPA (0.50 g per os) administration in seven patients affected by hypertension and secondary hyperaldosteronism. The results suggest that L-DOPA administration, by stimulating the dopaminergic biosynthesis. Nevertheless such a conclusion needs further investigations.

The Authors have studied, in a group of hypertensive subjects with low renin, the behavior of arterial blood pressure, PRA, plasma aldosterone, plasma K and Na, after intravenous load of Saralasin before and after treatment with Furosmide (40 mg orally given for 4 days). In such conditions we evidenced an agonist effect of Saralasin mainly on plasma aldosterone and less on arterial pressure. The Authors conclude that Saralasin, in given conditions (free receptor sites), can exhibit on agonist effect on aldosterone secretion; such agonist effect can be augmented by dopaminergic deficit, that sometimes in present is essential arterial hypertension.

PRA (in the supine and erect subject) and urinary sodium before and after acute treatment (100 mg i.m.) and chronic treatment (100 mg per os for 8 days) were examined in two groups of subjects with no signs of cardiovascular or renal disease. It was found that indomethacin, which is a well-known inhibitor of prostaglandin synthesis, reduced PRA levels in basal conditions and as a result of postural stimulation, without causing any appreciable change in urinary sodium. Regulation of the PRA on the part of the renal prostaglandins is postulated and its probable mechanisms discussed.

Angiotensin II increases aldosterone production of isolated and superfused bovine adrenal glands. Indomethacin shows a bi-phasic effect on the production of the above-mentioned hormone, inhibitory at low doses (0,2 microgram/ml), stimulatory at high doses (5.0 microgram/ml). Preincubation with this drug impedes the increase of aldosterone production induced by angiotensin II. It is likely that the steroidogenetic effect of angiotnesin II is carried out through the PGs.

Sulpiride induces an increase in plasma prolactin and a simultaneous increase of aldosterone release in man. In isolated and superfused bovine adrenal glands, prolactin does not increase aldosterone production even in high concentrations, whereas sulpiride induces a significant and long lasting increase in the production of this hormone and a concomitant increase in the tissue levels of cAMP. This suggests a direct effect on the biosynthesis of aldosterone.

The behaviour of aldosterone output was evaluated in isolated and superfused bovine adrenal glands during superfusion with human alpha atrial natriuretic peptide on its own or with angiotensin II or a antagonist dopaminergic drug: metoclopramide. H alpha-ANP even in high concentrations did not reduce the basal amount of aldosterone released from bovine adrenal glands, nor did it modify aldosterone response to metoclopramide, but it partially inhibited aldosterone stimulation by angiotensin II. These data suggest that atrial natriuretic factor may affect sodium secretion through the modulation of aldosterone secretion.

The effect of L-dopa (0.50 g, orally) on serum aldosterone, cortisol and potassium levels, plasma renin activity, and on urinary aldosterone excretion has been studied in normotensive subjects, before and after dexamethasone-induced ACTH suppression. L-dopa caused a further reduction in the levels of aldosterone but not cortisol, in the dexamethasone treated subjects. It is therefore suggested that the inhibitory action of L-dopa on aldosterone secretion is mediated by the dopaminergic system.

The authors studied the blood aldosterone, cortisol, and kalium levels, the plasma renin activity and the aldosterone urinary excretion following L-Dopa (0,50 g per os) administration in five patients affected by hypertension and six healthy control subjects, before and after the CRF-ACTH system suppression. The observed pattern shows that the aldosterone biosynthesis is inhibited also after the CRF-ACTH system has been suppressed. Therefore the authors conclude that the inhibiting action of L-Dopa on the aldosterone biosynthesis is mediated by the dopaminergic system stimulation.