Noradrenaline and ATP produce vasodilatation in the rabbit coronary artery by a direct action on the smooth muscle.
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 beta-adrenoceptor blockade, with a pD2 of 5.96 +/- 0.21. This was inhibited by 1 microM 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. 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 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 of 30 mM KCl. 4. We conclude that in the rabbit coronary artery both NA and ATP produce vasodilatation by a direct action on the smooth muscle.
Corr et al. (Tue,) reported a other. Noradrenaline (NA), adenosine, and adenosine 5'-triphosphate (ATP) was evaluated on Vasodilator and vasoconstrictor responses. Noradrenaline and ATP produce vasodilatation in the rabbit coronary artery by a direct action on the smooth muscle.