Aldosterone response to metoclopramide in patients with prolactinoma: effect of short-term bromocriptine treatment.

The acute effect of 10 mg metoclopramide i.v. on prolactin and aldosterone levels was studied in 8 women with prolactinoma and 8 normal women. The prolactin response to metoclopramide was blunted in hyperprolactinemic patients in comparison with controls. Metoclopramide induced similar aldosterone increases in patients and controls, but hyperprolactinemic women showed a more sustained aldosterone response. Bromocriptine treatment (10 mg daily p.o. for 5 days) in patients with prolactinoma completely suppressed the prolactin response to metoclopramide and the aldosterone response curve was very similar to that of controls. The results did not exclude some degree of suppression of aldosterone in response to bromocriptine.

Plasma aldosterone response to metoclopramide in patients with Cushing's disease.

The acute effect of metoclopramide on aldosterone and prolactin levels were studied in 8 control subjects and 11 patients with Cushing's disease. Metoclopramide (10 mg i.v.) induced a similar plasma prolactin response in control subjects and patients. No difference was found in basal aldosterone levels between the two groups. Apart from a more delayed aldosterone response to metoclopramide in the Cushing's disease group, no significant difference in the peak aldosterone values was found between the patients and controls. The short-term treatment with DA2-receptor agonist bromocriptine was without effect on aldosterone response to metoclopramide in the Cushing's disease group. These results argue against an altered dopaminergic control of aldosterone secretion in patients with Cushing's disease. The lack of a bromocriptine effect on aldosterone response to metoclopramide is in accordance with the concept that the dopamine receptors involved in aldosterone regulation differ from classical DA2 receptors.

Role of prostaglandin E2 (PGE2) on the corticotropin-releasing hormone (CRH)-induced ACTH release in healthy men.

The effect of PGE2 on ACTH and cortisol responses to CRH was studied in 6 healthy men who received CRH i.v. during either saline or PGE2 infusions which were started 60 min. before testing. ACTH and cortisol responses to CRH were greater during PGE2 infusion compared to the control study. The results indicate that PGE2 positively modulates CRH-induced ACTH secretion.

Serum aldosterone response to metoclopramide in normal subjects and acromegalic patients.

The acute effects of metoclopramide on aldosterone and prolactin levels were studied in 11 normal subjects, 8 normotensive and 8 hypertensive acromegalics. Metoclopramide (10 mg i.v.) induced a similar serum aldosterone increase in normal subjects and normotensive acromegalics. Hypertensive acromegalics showed elevated basal serum aldosterone level and blunted aldosterone response to metoclopramide. The prolactin response to metoclopramide was blunted in acromegalics in comparison with normal subjects but the difference was statistically significant only in hypertensive patients. The blunted aldosterone and prolactin responses to metoclopramide in hypertensive acromegalics suggest that there is a dopamine deficiency at central and adrenal level in these patients.

[Calcium-phosphorus metabolism and calcitrophic hormones in patients with active acromegaly with and without osteoporosis]. / Kaltsievo-fosforen obmen i kaltsitrofichni khormoni pri bolni s aktivna akromegaliia sus i bez osteoporoza,

Calcium-phosphor metabolism was studied in patients with active acromegaly with or without osteoporosis, mean age 45.2 +/- 11.4 years and mean duration of the basic disease 5.52 +/- 3.6 years. No significant deviations and no direct relation with the high serum growth hormone and prolactin levels were found. The normal basic secretion of the calcitrophic hormones--parathyroid hormone and calcitonin and their normal response to the hypercalcemia after intravenous calcium load of the patients with and without osteoporosis reject their direct participation in the pathogenesis of osteopenia. The changed skeletal sensitivity to calcitrophic hormones closely connected with the patients' age and the duration of the basic disease in combination with many other factors probably plays a major role in the pathogenesis of osteopenia.

Effect of verapamil on renin-angiotensin-aldosterone system, urinary 6-keto prostaglandin F1 alpha and aldosterone response to metoclopramide in normal man.

Seven healthy male volunteers were studied at the end of 7 days placebo period and after 7 days treatment with verapamil (120 mg twice daily). Verapamil increased significantly plasma renin activity and urinary excretion of 6-keto prostaglandin F1 alpha without significant modification of plasma aldosterone. Metoclopramide (10 mg i. v.) induced a significant increase of plasma aldosterone with the peak values 15 min after the injection of the drug. The results indicate that verapamil does not lead to secondary hyperaldosteronism which is characteristic of most other vasodilators. The increase of prostacyclin, measured as 6-keto prostaglandin F1 alpha can contribute to the efficacy of verapamil in patients with ischemic heart disease and hypertension. The present study suggests that the aldosterone response to metoclopramide is not directly dependent on calcium, but an indirect effect of calcium through renin-angiotensin system cannot be excluded.