Mechanical properties and effects of sympathetic co-transmitters on human coronary arteries and veins

Active isometric wall tension was studied at different levels of passive wall tension in isolated circular 2 mm long segments of human epicardial coronary arteries and veins, and maximum active wall tension was calculated to 6.60 mN/ mm for arteries and 0.86 mN/mm for veins. Vasomotor responses to sympathetic co-transmitters were studied at resting tension and after precontraction with U46619. Noradrenaline (NA) and adenosine 5-triphosphate (ATP) induced strong contractions of veins, whereas relaxant responses dominated in arteries. Isoprenaline potently relaxed all arteries and veins. Prazosin and rauwolscine in a concentration of 10^–7 M both competitively antagonized NA-induced contraction of arteries and veins. For uridine 5-triphosphate (UTP), relaxant responses were demonstrated in most arteries but only some veins. Neuropeptide Y (NPY) elicited no observable vasomotor responses in either arteries or veins. Mechanical removal of the arterial endothelium did not significantly alter relaxant responses to NA, ATP, UTP or isoprenaline. In conclusion, ₁-and ₂-adrenoceptors mediating contraction and -adrenoceptors mediating relaxation seem to be present in both human epicardial coronary arteries and veins. When applied to isolated epicardial coronary vessels, NA and ATP had a stronger influence on vasomotor tone than NPY and UTP, mediating strong contraction of veins but mainly relaxation of coronary arteries, that was independent of an intact endothelium.