AJP - Endocrinology and Metabolism, Vol 262, Issue 3 E312-E318, Copyright © 1992 by American Physiological Society
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 and N. Glorioso
Department of Clinical Medicine, Sassari University, Italy.
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 less than 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 less than 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 less than 0.05). The brain
kallikrein-kinin system may play a role in the regulation of ACTH secretion
in stimulated conditions.
