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, alpha 1- and alpha 2-adrenoceptors mediating contraction and beta-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.
Saetrum Opgaard
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Department of Internal Medicine, University Hospital of Lund, Sweden.
Edvinsson
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L
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001158:Arteries / Q000502:physiology; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008875:Middle Aged; D018377:Neurotransmitter Agents / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000378:metabolism*; D014661:Vasoconstriction; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology; D014666:Vasomotor System / Q000187:drug effects / Q000502:physiology; D014680:Veins / Q000502:physiology
D018377:Neurotransmitter Agents; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents