Dopaminergic Regulation of Aldosterone Secretion in Primary Aldosteronism: A Clinical Study.
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To assess the role of dopaminergic inhibition of aldosterone secretion in primary aldosteronism (PA) we studied the effect of dopaminergic DA2 blockade and stimulation in a series of consecutive cases of PA, and of primary hypertension (PH) as controls. Thirteen patients with confirmed PA (11 adenoma, 2 idiopathic hyperaldosteronism) and 8 primary hypertensive subjects (PH) were studied while on a 100 mmol/day sodium diet. Patients with aldosterone-producing adenoma were studied before, 1-2wk after, and 6 months after surgery. The DA2-antagonist metoclopramide (10mg i.v.) and the DA2-agonist dihydroergotoxine (6μg/Kg b.w. i.v.) were administered on different days. The effect of the latter on adrenal vein aldosterone and cortisol levels was also studied in selected cases. Plasma aldosterone, prolactin, cortisol, renin activity, free catecholamines, ACTH, Na+, K+, heart rate, and blood pressure were measured before and repeatedly after administration of each drug. In both groups, metoclopramide significantly increased aldosterone, prolactin, and cortisol (p<0.01), slightly decreased K+, and did not change the other variables. In PA patients, the aldosterone output was significantly (p<0.05) greater than in PH, and fell after surgery. There was no difference, however, in responsiveness to metoclopramide between PA and control patients. Dihydroergotoxine significantly decreased plasma prolactin and aldosterone levels and adrenal vein aldosterone in patients with PH. In contrast, despite a similar decrease in prolactin, in PA a significant (p<0.05) increase in aldosterone was seen, both peripherally and in adrenal vein blood. Thus, in PA: 1) the response to DA2 blockade is qualitatively normal but quantitatively enhanced; 2) this enhancement disappears after removal of the adenoma and thus appears related to increased aldosterone-secreting tissue rather than to enhanced responsiveness; 3) the response stimulation by dihydroergotoxine is paradoxical in PA, and may be mediated through ACTH stimulation. (Hypertens Res 1994; 17: 105-115)
- 日本高血圧学会の論文
日本高血圧学会 | 論文
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