BROMOCRIPTINE: LACK OF EFFECT ON THE ANGIOTENSIN II AND ALDOSTERONE RESPONSES TO SODIUM DEPRIVATION

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Abstract
Five normal subjects took a low sodium diet for four days on two occasions, one with and one without added bromocriptine 2.5 mg three times a day by mouth. Daily measurements of urinary electrolytes and the concentrations of plasma renin (PRC), angiotensin II (AII), aldosterone, 18-hydroxycorticosterone, cortisol, electrolytes and prolactin were made in both phases of the study. Deprivation of sodium without bromocriptine resulted in progressive and highly significant increases in the plasma concentration of aldosterone from 230 ± 50 to 418 ± 44 (SEM) pmol/l, 18-hydroxycorticosterone from 627 ± 138 to 1420 ± 478 pmol/l, PRC from 108 ± 38 to 166 ± 14 μU/ml and AII from 16 ± 3 to 29 ± 4 pmol/l. Similar changes were found during bromocriptine administration despite suppression of prolactin secretion. Sodium deprivation together with bromocriptine resulted in increases in the plasma concentrations of aldosterone from 230 ± 47 to 416 ± 72 pmol/l, 18-hydroxycorticosterone from 630 ± 99 to 1629 ± 552 pmol/l, PRC from 105 ± 12 μU/ml and AII from 14 ± 3 to 26 ± 5 pmol/l. Plasma cortisol did not change either in response to sodium deprivation or bromocriptine. Mean cumulative negative sodium balance was 101 ± 14 mmol on bromocriptine and 118 ± 14 mmol in the control period. We conclude that prolactin is not necessary for the steroidogenic response to sodium deprivation in man.