Are Plasma Aldosterone Surges in Primary Aldosteronism due to a Loss of an Inhibitory Dopaminergic Control?*

To evaluate the interrelationship between plasma aldosterone (PA) and dopamine (DA) in primary aldosteronism we determined their correlations during nycthemeral cycles (before and after dexamethasone), as well as during postural or episodic increases in PA in four patients. Plasma cortisol and PRL were also determined. There was an overall negative correlation between plasma DA on the one hand and PA, PRL, and cortisol on the other, the latter three being positively correlated with one another. The strongest positive relationship was between aldosterone and cortisol; the strongest negative correlation was between PRL and free DA. Dexamethasone administration suppressed PA to 70 ± 6%, PRL to 71 ± 5%, and cortisol to 24 ± 2% of the previous levels (100%), and increased plasma free DA to 260 ± 49%. During the first 12 h ofthe cycle, corresponding to PA suppression by dexamethasone, the positive correlation between PA and plasma cortisol strengthened, and a positive correlation of plasma cortisol with PRL appeared; both disappeared in the second 12 hcorresponding to the escape of PA from the inhibitory action of dexamethasone. In a patient with periodic hyperaldosteronism in 8– to 10-day cycles, lower PA and normokalemia were associated with a huge increase in plasma conjugated DA; when plasma conjugated DA was low, it was associated with high PA and low potassium levels. The observation of elevated plasma DA suggests that the dopaminergic inhibitory pathway of aldosterone is activated in primary aldosteronism. Opposing fluctuations in PA, PRL, and cortisol on the one hand and plasma DA on the other, spontaneously or during dexamethasone administration, are compatible with the hypothesis that a weakening of dopaminergic inhibitory control contributes to the otherwise unexplained PA surges, while an increase in DA contributes to the dexamethasoneinduced suppression of PA; the positive correlation of plasma cortisol with PA and PRL suggests that this inhibitory action of DA may be mediated in the first 12 h by suppression of ACTH secretion but later may act independently of it.