The renin-angiotensin-aldosterone axis in patients with nontumoral [corrected] hyperprolactinemia

Objective In physiological conditions, renin–angiotensin–aldosterone (RAA) axis is under continuous tonic inhibition by dopamine. The aim of this study was to evaluate the relationship of nontumoural hyperprolactinemia with the activity of adrenocortical and RAA axis, before and after administration of bromocriptine. Design Twenty women with nontumoural hyperprolactinemia and 20 healthy women matched for body mass index and age were recruited in this study. All participants were placed on fixed salt intake for 2 weeks before the experiments. The study was conducted in three phases. In phase I, the participants received an intravenous infusion of angiotensin II in three consecutive doses of 2, 4 and 6 ng/kg BW changed every 30 min. In phase II, the patients were started on bromocriptine in gradually increasing doses of 1·25, 2·5, 5, 7·5 and 10 mg/day for 10 weeks. In phase III, the protocol of phase I was repeated in the patient group. Circulating levels of cortisol, plasma renin activity (PRA), aldosterone and prolactin were assayed. Results Baseline values of prolactin, and PRA (2·6 ± 0·18 nm vs 0·45 ± 0·05 nm P < 0·001 and 142·2 ± 14·4 vs 30·7 ± 2·7 pm /h, P < 0·001, respectively) but not aldosterone (P = 0·081) were significantly higher in the patient group. The angiotensin infusion test induced a significantly greater response in the patient group. Administration of the dopamine agonist restored the basal levels and diminished the response to angiotensin infusion for all the parameters tested. No change in the blood pressure was recorded. Conclusions Our study demonstrates that in nontumoural hyperprolactinemia there is an increased reactivity of renin–angiotensin–aldosterone (RAA) axis that is almost completely restored after treatment with a dopamine agonist.