A factor released from coronary vascular endothelium inhibits myocardial contractile performance.

The effect of continuous intracoronary infusion of bradykinin (BK; 10(-6) M) on the myocardial contractile performance of isolated Langendorff-perfused ferret hearts was investigated. BK produced a transient but marked inhibition of contractile performance, the changes being fully resolved by 2-3 min. This effect of BK was blocked after disruption of the coronary vascular endothelium with Triton X-100 (0.5%). Prior infusion of the endothelium-derived relaxing factor (EDRF) synthesis inhibitor N omega-nitro-L-arginine (10(-4) M) failed to alter the mechanical effects induced by BK. These changes in contractile performance were reduced, however, by the K+ channel-blocking agent glibenclamide (10(-6) M) but were unaffected by tetrapentylammonium bromide (5 x 10(-5) M) or 4-aminopyridine (10(-3) M). These findings therefore indicate that BK inhibits myocardial contractile performance by opening myocardial ATP-sensitive K+ channels, probably via the release of an endothelium-derived factor unrelated to EDRF.