Aldosterone responses to angiotensin II, adrenocorticotropin, and potassium in chronic experimental diabetes mellitus in rats

M. Hayashi, W. Kitajima, T. Saruta

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Abstract

To investigate alterations in aldosterone secretion in diabetes mellitus, the effects of angiotensin II, ACTH, and potassium on aldosterone secretion were examined in conscious unrestrained streptozotocin-induced diabetic rats (60 mg/kg, 12 weeks before study). In chronic experimental diabetic rats where PRA, plasma aldosterone concentration, and urinary excretion of prostaglandin E2 were significantly decreased, a significant attenuated response of aldosterone secretion was demonstrated after infusion of angiotensin II, ACTH, or potassium. Yet the plasma fluorogenic corticosteroids response to ACTH in diabetic rats was not significantly different from that in control rats. After acute potassium infusion (0.30 meq/kg·min), plasma potassium levels in diabetic rats were significantly higher than in control rats, although immunoreactive insulin levels remained unchanged compared to the significant elevation in control rats. These results suggest that defects in aldosterone synthesis exist in chronic experimental diabetic rats and that potassium homeostasis is impaired during acute potassium loading. This change in potassium homeostasis may be related to both insulin and aldosterone deficiencies.

Original languageEnglish
Pages (from-to)2205-2209
Number of pages5
JournalEndocrinology
Volume115
Issue number6
Publication statusPublished - 1984

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Experimental Diabetes Mellitus
Aldosterone
Angiotensin II
Adrenocorticotropic Hormone
Potassium
Homeostasis
Insulin
Streptozocin
Dinoprostone
Diabetes Mellitus
Adrenal Cortex Hormones

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Aldosterone responses to angiotensin II, adrenocorticotropin, and potassium in chronic experimental diabetes mellitus in rats. / Hayashi, M.; Kitajima, W.; Saruta, T.

In: Endocrinology, Vol. 115, No. 6, 1984, p. 2205-2209.

Research output: Contribution to journalArticle

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