COLLATERAL RESPONSE TO ACTIVATION OF POTASSIUM CHANNELS IN-VIVO

Activation of ATP-sensitive K+ channels is involved in the coronary va scular response to decreases in perfusion pressure and ischemia. Since activation of ATP-sensitive K+ channels in collateral vessels may be important in determining flow to collateral-dependent myocardium, the ability of collaterals to respond to activation of the channel was tes ted. In the beating heart of dogs, we compared responses of non-collat erals less than 100 mu m in diameter to collaterals of similar size us ing computer-controlled stroboscopic epi-illumination of the left vent ricle coupled to a microscope-video system. Aprikalim, a selective act ivator of ATP-sensitive K+ channels (0.1-10 mu M) produced similar dos e-dependent dilation of non-collaterals and collaterals. Relaxation wa s decreased by inhibition of ATP-sensitive K+ channels with glibenclam ide, but not by inhibition of nitric oxide synthase with nitro-L-argin ine. Bradykinin (10-100 mu M) produced similar dilation of non-collate rals and collaterals which was decreased by nitro-L-arginine but not g libenclamide. Thus, in microvascular collaterals, relaxation to both n itric oxide and activation of ATP-sensitive K+ channels is similar to non-collaterals.