Electrical stimulation caused frequency-dependent reversible relaxations of canine coronary arteries made to contract with prostaglandin F2α, phenylephrine, 5-hydroxytryptamine, potassium chloride, or angiotensin II. These contractions were not affected by cold storage, tetrodotoxin, α- and β-adrenergic blockade and atropine, demonstrating that they probably are not due to activation of inhibitory nerves. The relaxations persisted in the presence of indomethacin and after removal of the endothelium. They were not seen in splenic arteries and saphenous veins, demonstrating the high sensitivity of the coronary blood vessel wall to the inhibitory effects of the electric impulses.
- Coronary smooth muscle
- Electrical stimulation
- Inhibitory vasodilator nerves
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