Effects of the kallikrein-kinin system on phasic coronary vasospasm in dogs

It is well known that kinins are liberated from kininogen in blood during angina attack to maintain blood flow in coronary artery. We examined the effects of bradykinin, one of kinins, on the coronary artery other than vasodilation. The isolated canine coronary artery ring was suspended in gassed (95% O2, 5% CO2) Krebs-Henseleit buffer at 37 degrees C in vitro. The experimental phasic contraction of coronary artery was induced by 6 x 10(-4)M of 3,4-diaminopyridine which decreases K conductance (Y. Uchida, Jpn. Circ. J: 49, 128, 1985). The effect of bradykinin and other substances on the cycle length of contraction (CL), the peak tension of contraction phase (PT) and the tension during relaxation phase (RT) were observed. The phasic contraction was eliminated by 10(-7)M nifedipine and 10(-6)M diltiazem which block voltage dependent Ca channels. These Ca blockers reduced PT, but slightly increased CL, and weakly reduced RT. The phasic contraction was also eliminated by 10(-6)M bradykinin. However, bradykinin, unlike Ca blockers, did not reduce PT, but markedly prolonged CL and decreased RT significantly. This inhibition mode was very similar to those of nicorandil which increases K conductance. These data suggest that bradykinin plays a protective role in coronary vasospasm, and this antivasospasm effect may be mediated through the increase in K conductance.