Aldosterone suppression with dopamine infusion in low-renin hypertension.
A dopaminergic mechanism has been proposed to suppress aldosterone secretion. To assess the possibility that a defect in the dopaminergic mechanism might enhance aldosterone secretion in hypertensive patients, we determined basal and adrenocorticotropic hormone (ACTH)-stimulated plasma aldosterone (PA), cortisol, renin activity, and potassium concentrations before and during dopamine receptor stimulation with dopamine infusion and bromocriptine administration and dopamine receptor blockade with metoclopramide. The patient study groups included: (a) seven patients with low-renin hypertension and abnormal aldosterone suppression with sodium loading and presumed bilateral zona glomerulosa hyperplasia (ZGHP); (b) two patients with aldosterone-producing adenoma; (c) five patients with low-renin hypertension but normal aldosterone suppression with sodium loading; and (d) six patients with normal-renin hypertension. Dopamine infusion in patients with ZGHP caused PA to fall (P less than 0.01) into the normal range, but did not block the enhanced (P less than 0.05) aldosterone response to ACTH that is characteristic of these patients. Dopamine infusion in patients with low-renin hypertension but normal aldosterone suppression also suppressed PA (P less than 0.01), whereas it had no effect upon PA in patients with normal-renin hypertension or aldosterone-producing adenoma and did not blunt the PA response to ACTH in either group. Bromocriptine administration had no effect upon basal or ACTH-stimulated PA. Dopamine infusion in patients with ZGHP also enhanced (P less than 0.05) diuresis and natriuresis in comparison with normal-renin patients. Metoclopramide administration increased (P less than 0.01) PA in all patients. Thus, a dopaminergic mechanism appears to be important in the regulation of aldosterone secretion in patients with ZGHP and in other low-renin hypertensives with normal aldosterone suppression with sodium loading. In contrast, this latter group does not exhibit an enhanced aldosterone response to ACTH. Both of these groups differ from normal-renin hypertensives, who have no PA suppression with dopamine infusion.
D000236:Adenoma / Q000378:metabolism; D000310:Adrenal Gland Neoplasms / Q000378:metabolism; D000311:Adrenal Glands / Q000473:pathology; D000324:Adrenocorticotropic Hormone / Q000008:administration & dosage; D000328:Adult; D000450:Aldosterone / Q000097:blood*; D001971:Bromocriptine / Q000008:administration & dosage; D004231:Diuresis / Q000187:drug effects; D004298:Dopamine / Q000008:administration & dosage* / Q000097:blood; D004305:Dose-Response Relationship, Drug; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006965:Hyperplasia / Q000378:metabolism; D006973:Hypertension / Q000378:metabolism*; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000008:administration & dosage*; D012083:Renin / Q000097:blood
D000451:Mineralocorticoid Receptor Antagonists; D001971:Bromocriptine; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D012083:Renin; D004298:Dopamine; D006854:Hydrocortisone