Kinin B 2 receptor‐mediated contraction of tail arteries from normal or streptozotocin‐induced diabetic rats

1 The vasoactive effects of bradykinin (BK) are mediated by different subtypes of kinin receptors, of which the expression varies among different tissues. In rat tail artery tissues, BK elicited a concentration‐dependent vasoconstriction (EC50, 25.9±2.4 n M ; Emax, 0.39±0.01 g; n =16). This effect of BK was endothelium independent and indomethacin insensitive. The BK‐induced contraction of tail artery tissues, however, depended on both membrane potential‐sensitive extracellular Ca 2+ entry and thapsigargin‐sensitive intracellular Ca 2+ release. 2 Kinin B 1 receptor antagonist or agonist did not affect the basal tension or the BK‐induced contraction of tail artery tissues in the absence or presence of endothelium ( P >0.05 ). In contrast, the BK‐induced vasoconstriction was inhibited by kinin B 2 receptor antagonists. Pretreatment of vascular tissues with Hoe 140 (1 n M ) significantly changed EC50 of the BK‐induced vasoconstriction from 25.5±7.4 n M to 82.6±16.8 n M ( n =8, P <0.01 ) and Emax from 0.43±0.03 g to 0.16±0.01 g ( n =8, P <0.01 ). 3 In the tail artery tissues from streptozotocin‐induced diabetic rats, the BK‐elicited vasoconstriction was significantly reduced (EC50, 67.8±11 n M ; Emax, 0.19±0.01 g) compared to their counterparts from normal rats. The decreased vasoconstrictive effects of BK on diabetic arteries were endothelium independent and indomethacin insensitive. 4 Our study demonstrated that the contraction of rat tail arteries induced by BK was mediated by B 2 receptors located on vascular smooth muscles. The altered B 2 receptor‐mediated vascular activity may play an important role in the vascular complications of diabetes.British Journal of Pharmacology (1998) 125 , 143–151; doi: 10.1038/sj.bjp.0702017