Mechanisms involved in relaxation induced by exogenous nitric oxide in pig coronary arteries

The aim of the present study was to analyze the mechanisms involved in the vasodilator responses elicited by nitric oxide (NO) in segments of porcine posterior descending coronary artery. Exogenous NO (0.1-30 μM) induced concentration-dependent relaxations in segments precontracted with a concentration of the thromboxane A 2 mimetic, U-46619 (30-300 nM) that produced a contraction 70% (submaximal contraction) of that elicited by 75 mM K + (maximal contraction). The relaxations were almost abolished by 6-anilinoquinoline-5,8-quinone (LY-83583, 10 μM), an inhibitor of guanylate cyclase, and with precontraction with 40 or 60 mM K + . Relaxations were reduced by 5 mM tetraethylammonium (TEA), a blocker of Ca 2+ -activated K + channels (K Ca channels) and unaltered by ouabain (500 μM), 4-aminopyridine (1 mM), glibenclumide (10 μM). apamin (1 μM) and charybdotoxin (0.3 μM), inhibitors of sodium pump, voltage-sensitive, ATP-sensitive, small-conductance K Ca and large-conductance K Ca K + channels, respectively. These results suggest that the relaxation caused by exogenous NO is mediated by guanylate cyclase activation, with only a slight participation of a hyperpolarizing mechanism mediated by activation of K Co channels.