In:
Acta Endocrinologica, Oxford University Press (OUP), Vol. 103, No. 3 ( 1983-07), p. 391-399
Abstract:
Abstract. A possible role of corticotrophin in mediating the acute glucose-induced suppression of plasma aldosterone was assessed in two groups of normal subjects (group A, N = 9 and group B, N = 10), by studying the effects of a standard oral glucose loading test on plasma concentrations of glucose, insulin, cortisol, potassium, aldosterone and renin activity, a) under basal conditions (groups A and B), b) after 2 days of dexamethasone (0.5 mg/6 h) (group A), c) after 8 weeks of treatment with the diuretic indapamide, 2.5 mg/day (group B) and d) after additional 2 days of combined administration of indapamide and dexamethasone (0.5 mg/6 h) (group B). In addition, the spontaneous daytime related variations of these parameters were assessed in group A in a control study without glucose loading. Under basal conditions, the acute increase in plasma glucose and insulin was accompanied by a significant decrease of plasma potassium ( P 〈 0.01), cortisol ( P 〈 0.01) and by a slight increase in plasma renin activity. None of these changes occurred in the control experiment without glucose loading. Dexamethasone caused a significant decrease in pre-loading plasma aldosterone. Indapamide caused a significant decrease in pre-loading plasma potassium and a marked stimulation of renin and aldosterone. After combined indapamide-dexamethasone administration, pre-loading plasma aldosterone decreased to control values. Glucose loading under dexamethasone or combined indapamide-dexamethasone administration caused a similar suppression of plasma aldosterone as observed under control conditions. These findings suggest that corticotrophin does not play an important role in mediating the acute aldosterone inhibitory effect of glucose loading. However, corticotrophin may contribute to the maintenance of the secondary hyperaldosteronism induced by diuretic treatment.
Type of Medium:
Online Resource
ISSN:
0804-4643
,
1479-683X
DOI:
10.1530/acta.0.1030391
Language:
Unknown
Publisher:
Oxford University Press (OUP)
Publication Date:
1983
detail.hit.zdb_id:
1183856-5
detail.hit.zdb_id:
1485160-X
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