Vasodilator response of coronary smooth muscle to the sympathetic co‐transmitters noradrenaline and adenosine 5′‐triphosphate

Abstract

1 Vasodilator and vasoconstrictor responses to noradrenaline (NA), adenosine and adenosine 5'-triphosphate (ATP) were examined in isolated ring segments of the left anterior descending coronary artery of the rabbit in the absence of endothelium.2 NA caused dose-dependent relaxation of potassium-constricted vessels in the absence of aladrenoceptor blockade, with a pD2 of 5.96 + 0.21. This was inhibited by 1 gM propranolol. Constrictor responses of vessels at baseline tension were only seen at concentrations greater than 1 mm, and reached a maximum of 6% of the contraction to 30 mm KCI. 3 ATP caused relaxation of the potassium-constricted ring segments in a dose-dependent manner, although a transient constriction often preceded the relaxation. Adenosine was equipotent with ATP in producing relaxation; this was significantly inhibited by the Pl-purinoceptor antagonist, 8-phenyltheophylline (8-PT). The responses to ATP were little affected by 8-PT, indicating that ATP was not acting through breakdown to adenosine. At basal tone, ATP produced transient vasoconstriction only at concentrations greater than 0.1 mm, reaching a maximum of 38% of the contraction to 30mM KCl. 4 We conclude that in the rabbit coronary artery both NA and ATP produce vasodilatation by a direct action on the smooth muscle.

Role of A2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart

“…Studies on isolated vessels and isolated hearts support the view that ATP causes coronary vasodilation by P 2Y receptor activation (Brown et al, 1992;Corr & Burnstock. 1991;Fleetwood & Gordon, 1987;Gordon, 1986;Hopwood & Burnstock, 1987;Matsumoto et al, 1997;Olsson & Pearson, 1990;Simonsen et al, 1997;Vials & Burnstock, 1994;Godecke et al, 1996).…”

Purinergic Signaling and Blood Vessels in Health and Disease

“…The possibility is raised that this may be important for thermoregulation and may explain why purinergic cotransmission is more prominent in cutaneous compared with deep blood vessels. NA and ATP act as vasoconstrictors to most blood vessels via a-adrenoceptors and P2X 1 purinoceptors; studies carried out on the rabbit coronary artery, where the predominant effect of NA is vasodilation via b-adrenoceptors, have shown that the cotransmitter ATP causes vasodilation via muscle P2Y purinoceptors (Corr and Burnstock, 1991;Keef et al, 1992).…”

Immunolocalization of the Ecto-ATPase and Ecto-apyrase in Chicken Gizzard and Stomach

“…Extracellular nucleotides have been implicated in many important physiological processes (1), including purinergic signaling in smooth muscle (2,3), neurotransmission (4,5), cell adhesion, apoptosis (6), and platelet aggregation and clotting (7). Enzymes for hydrolyzing extracellular nucleotides, including ecto-ATPases and ecto-apyrases (which we call collectively ecto-ATP(D)ases), have been implicated in termination of purinergic stimulation of muscle (2,8), termination of pain transmission (4), parasite adaptations to host defenses (9), as well as important regulators of thrombotic processes and in maintaining hemostasis in the circulatory system (7,10).…”