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THE RELATIONSHIP BETWEEN ENDOGENOUS HYPERPROLACTINAEMIA AND PLASMA ALDOSTERONE

It has been suggested that prolactin is a regulator of aldosterone secretion. In order to test this hypothesis, we measured prolactin, thyrotrophin and aldosterone by radioimmunoassay and plasma renin activity by the radioimmunoassay of angiotensin I in eight normal women before and after the intravenous injection of 200 μg of thyrotrophin releasing hormone (TRH). Prolactin increased from 4.1 ± 1.1 ng/ml (mean ± SE) to a peak of 27.4 ± 3.8 (P > 0.005) at 15 min following TRH. Plasma renin activity was not different from control levels (1.0 ± 0.2 ng/ml/h) during the first hour following the administration of TRH, nor did the plasma aldosterone concentration differ significantly from the control levels (39 ± 7 pg/ml) during this period. However, with upright posture, an increase in aldosterone (from 31 ± 3 pg/ ml at 1 h to 68 ± 9 at 2 h, P > 0.005) and in plasma renin activity (from 0.9 ± 0.2 ng/ml/h at 1 h to 2.0 ± 0.5 at 2 h, P > 0.05) was noted, demonstrating a normal capacity to secrete aldosterone in these subjects. Similarly, no change in aldosterone was seen in nine patients with primary hypothyroidism given TRH, despite the fact that the increase in prolactin was greater than normal. Chronic hyperpro‐lactinaemia was not associated with hyperaldosteronism in six patients with pituitary tumour. These data demonstrate that acutely or chronically elevated serum prolactin levels do not result in increased plasma aldosterone levels in humans.