Kinin B₂ 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 nM; 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 Ca²⁺ entry and thapsigargin-sensitive intracellular Ca²⁺ release.
• 2
  Kinin B₁ 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 B₂ receptor antagonists. Pretreatment of vascular tissues with Hoe 140 (1 nM) significantly changed EC50 of the BK-induced vasoconstriction from 25.5±7.4 nM to 82.6±16.8 nM (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 nM; 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 B₂ receptors located on vascular smooth muscles. The altered B₂ 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