Responses of canine coronary arteries to transmural electrical stimulation and nicotine.
In helical strips of dog coronary arteries contracted with prostaglandin F2 alpha, transmural electrical stimulation and nicotine elicited a transient relaxation. The response to electrical stimulation was abolished by tetrodotoxin, bretylium or pretreatment of the dogs with reserpine, and was potentiated by cocaine. Atropine was ineffective. The relaxations were abolished or converted to contractions by sotalol; the contraction was suppressed by phentolamine. The nicotine-induced relaxation was suppressed by hexamethonium, cocaine, bretylium and sotalol. Atropine and tetrodotoxin did not affect the response. Following pretreatment with reserpine, relaxant responses to nicotine were partly reduced; the remaining relaxations were suppressed by atropine, slightly inhibited by sotalol and potentiated by physostigmine. It may be concluded that electrical stimulation liberates norepinephrine from adrenergic nerves, which preferentially activates beta-adrenoceptors. The reuptake mechanism appears to function to inactivate liberated norepinephrine. Nicotine-induced relaxations are mediated mainly by liberated norepinephrine; however, as shown by the pretreatment with reserpine, the release of an acetylcholine-like substance may also be involved.
D000818:Animals; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D015237:Dinoprost; D004285:Dogs; D004558:Electric Stimulation; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D009538:Nicotine / Q000494:pharmacology*; D009638:Norepinephrine / Q000378:metabolism / Q000494:pharmacology; D011460:Prostaglandins F / Q000494:pharmacology; D012110:Reserpine / Q000494:pharmacology
D011460:Prostaglandins F; D009538:Nicotine; D012110:Reserpine; D015237:Dinoprost; D009638:Norepinephrine