Role of brain kallikrein-kinin system in regulation of adrenocorticotropin release

P. Madeddu, V. Anania, S. Alagna, C. Troffa, P. P. Parpaglia, G. Tonolo, M. P. Demontis, M. V. Varoni, C. Fattaccio, N. Glorioso

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Abstract

We evaluated whether the brain kallikrein-kinin system plays a role in the regulation of adrenocorticotropin (ACTH) release in rats. Intracerebroventricular (icv) injection of bradykinin (0.24 nmol) increased plasma immunoreactive ACTH (irACTH) levels (from 93 ± 4 to 200 ± 12 pg/ml, P <0.01). This effect was prevented by icv kinin antagonist at 15.4 nmol/h (from 98 ± 5 to 108 ± 6 pg/ml; not significant). The antagonist did not alter the increase in plasma irACTH levels induced by icv corticotropin- releasing factor (CRF), arginine vasopressin, or prostaglandin E2. Melittin (7 nmol/h icv) increased plasma irACTH from 95 ± 4 to 268 ± 7 pg/ml (P <0.01). This effect was prevented by icv kinin antagonist (15.4 nmol/h), kallikrein antibodies (13 pmol/h), or indomethacin (0.28 mmol/h). ACTH response to melittin was not altered by antagonists of CRF or vasopressin. Intra-arterial injection of insulin (0.3 IU/kg body wt) reduced plasma glucose levels to a similar extent in rats given icv kinin antagonist or vehicle; the ACTH response to insulin-induced hypoglycemia was slightly less in rats given kinin antagonist than in those given vehicle (55 ± 5 vs. 86 ± 4 pg/ml, P <0.05). The brain kallikrein-kinin system may play a role in the regulation of ACTH secretion in stimulated conditions.

Original languageEnglish
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume262
Issue number3 25-3
Publication statusPublished - 1992

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Keywords

  • melittin
  • pituitary

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology

Cite this

Madeddu, P., Anania, V., Alagna, S., Troffa, C., Parpaglia, P. P., Tonolo, G., Demontis, M. P., Varoni, M. V., Fattaccio, C., & Glorioso, N. (1992). Role of brain kallikrein-kinin system in regulation of adrenocorticotropin release. American Journal of Physiology - Endocrinology and Metabolism, 262(3 25-3).