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

Abstract

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. NA caused dose‐dependent relaxation of potassium‐constricted vessels in the absence of β‐adrenoceptor blockade, with a pD2 of 5.96 ±0.21. This was inhibited by 1 μm 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 KCl. 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 P1‐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 30 mm KCl. We conclude that in the rabbit coronary artery both NA and ATP produce vasodilatation by a direct action on the smooth muscle. 1991 British Pharmacological Society