Pharmacological Analysis of the Rat Femoral Artery Response to Bradykinin

Bradykinin (BK) plays an important role in different physiological processes including the general preservation and modulation of vascular systems. The present study was designed in order to examine the effect of BK on isolated rat femoral artery rings and to investigate the participation of intact endothelium, cyclooxygenase products, Ca(2+) channels, Na(+)/K(+)–ATPase, and B(2) kinin receptors in BK-induced action. Circular artery segments were placed in organ baths. The endothelium was mechanically removed from some arteries. Concentration–contraction curves for BK were obtained in the rings previously equilibrated at the basal tone. BK produced a concentration–dependent contraction, which was reduced by endothelial denudation. The BK–induced effect was almost completely inhibited by indomethacin (cyclooxygenase inhibitor) or OKY–046 (thromboxane A(2)–synthase inhibitor). Nifedipine (Ca(2+) channel blocker), ouabain (Na(+)/K(+)–ATPase inhibitor), or HOE–140 (selective B(2) kinin receptor antagonist) significantly reduced the BK–evoked effect. In conclusion, it can be proposed that BK produces concentration– and endothelium–dependent contractions of the isolated rat femoral artery, which is for the most part a consequence of B(2) kinin receptor activation. Cyclooxygenase contractile products, especially thromboxane A(2), play a significant role in this course of action. The transduction mechanism involved in the process of BK–induced femoral artery contraction include the activation of voltage–gated Ca(2+) channels, and in a smaller extent Na(+)/K(+)–ATPase as well.