Changes in blood glucose and plasma insulin levels induced by bradykinin in anaesthetized rats

Citation
J. Damas et al., Changes in blood glucose and plasma insulin levels induced by bradykinin in anaesthetized rats, BR J PHARM, 134(6), 2001, pp. 1312-1318
Citations number
40
Categorie Soggetti
Pharmacology & Toxicology
Journal title
BRITISH JOURNAL OF PHARMACOLOGY
ISSN journal
00071188 → ACNP
Volume
134
Issue
6
Year of publication
2001
Pages
1312 - 1318
Database
ISI
SICI code
0007-1188(200111)134:6<1312:CIBGAP>2.0.ZU;2-Y
Abstract
1 The influence of bradykinin (BK) on blood glucose and plasma insulin leve ls was investigated in anaesthetized rats. 2 Blood glucose level was dose-dependently increased by intravenous infusio n of BK. This effect of BK was enhanced by captopril, an inhibitor of angio tensin-converting enzyme (ACE). Des-Arg(9)-bradykinin (DABK), a kinin B-1 r eceptor agonist, did not modify blood glucose levels while the effect of BK was inhibited by Hoe-140, a kinin B-2 receptor antagonist. The effect of B K was reduced by the NO-synthase inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME), and by the cyclo-oxygenase inhibitor, indomethacin. 3 The effect of BK was suppressed by the association of propranolol with ph entolamine or phenoxybenzamine. It was also reduced by hexamethonium, a gan glion-blocking drug. In adrenalectomized rats, the infusion of BK slightly decreased blood glucose levels. 4 The hyperglycaemic effect of adrenaline was suppressed by propranolol ass ociated with phentolamine or phenoxybenzamine, but it was not modified by L -NAME. 5 Infusion of BK did not modify plasma insulin levels. However, after phent olamine and propranolol, BK induced a transient 2 fold rise in plasma insul in levels. The release of insulin was dose-dependent and inhibited by Hoe-1 40. 6 We conclude that infusion of BK induces, via a stimulation of B-2 recepto rs, the release of NO and of prostanoids. The latter agents activate throug h a reflex pathway the release of catecholamines from the adrenal medulla. This release increases blood glucose levels and reduces plasma insulin leve ls. After adrenoceptor inhibition, BK induces a secretion of insulin, via t he stimulation of B-2 receptors.