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  • Title: Endothelium-derived nitric oxide as a mediator of acetylcholine-induced coronary vasodilation in dogs.
    Author: Ishizaka H, Okumura K, Yamabe H, Tsuchiya T, Yasue H.
    Journal: J Cardiovasc Pharmacol; 1991 Nov; 18(5):665-9. PubMed ID: 1723762.
    Abstract:
    To investigate the role of endothelium-derived nitric oxide (NO) in regulation of the tonus of the coronary artery system in vivo, the effect of NG-mono-methyl-L-arginine (L-NMMA), a specific inhibitor of the synthesis of NO from L-arginine, on acetylcholine (ACh)-induced coronary vasodilation was examined in open-chest, anesthetized dogs. At baseline, the infusion of ACh and adenosine into the left circumflex coronary artery (LCX) increased the LCX blood flow. Continuous infusion of L-NMMA (2 mumol/min, for 20 min) into LCX significantly attenuated ACh-induced increase in the LCX flow: percentage increases in the LCX flow by ACh (10 and 100 ng/kg) before L-NMMA were 42.0 +/- 8.7 and 137.3 +/- 12.5%, respectively, whereas those after L-NMMA were 14.0 +/- 4.9 (p less than 0.02) and 88.9 +/- 10.9% (p less than 0.005), respectively. L-NMMA showed no effect on adenosine-induced increase in the LCX flow. After the L-NMMA infusion was terminated, the effect of ACh partially returned to the baseline level. In other dogs, L-arginine (3 mg/min, for 20 min) was administered just after the L-NMMA infusion, which completely reversed the inhibitory effect of L-NMMA on ACh-induced vasodilation. Endothelium-derived NO is a mediator of ACh-induced vasodilation of the coronary resistance vessels in dogs.
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