Abstract
Intravenous and intraarterial injections of epinephrine and electrical stimulation of the cervical sympathetic nerve were found to produce an increase in tension in the striated superior rectus muscle of the cat anesthetized with pentobarbital. Similar results were obtained from the smooth muscle of the ipsilateral nictitating membrane. The sympathetic beta-receptor blocking agents, pronethalol (5 mg/kg i.v.) and propranolol (1 mg/kg i.v.), did not antagonize these responses. In contrast, the alpha-receptor blocking agents, phenoxybenzamine (1-2 mg/kg i.v.) and phentolamine (2-3 mg/kg i.v.), abolished the responses of both muscles to epinephrine and sympathetic stimulation. Cocaine (5 mg/kg i.v.) potentiated the responses of both muscles to epinephrine and postganglionic sympathetic stimulation. A major difference between the two muscles occurred in their response to epinephrine after atropine (0.5-10 mg/kg i.v.). The responses of the superior rectus muscle and the nictitating membrane to sympathetic stimulation and the response of the nictitating membrane to epinephrine were depressed by atropine, whereas the response of the superior rectus muscle was unaffected. Intravenous injections of d-tubocurarine (1-2 mg/kg i.v.) were found to depress the responses of both muscles to small doses of epinephrine (0.1-0.5 µ/kg i.v.) but the responses to larger doses (5-10 µ/kg) were not depressed. It was concluded that the response of the superior rectus muscle to epinephrine did not correspond to the effect of the amine on chronically denervated mammalian striated muscles. Possible mechanisms of action of epinephrine and sympathetic stimulation on the superior rectus muscle are discussed.
Footnotes
- Received January 31, 1967.
- Accepted April 28, 1967.
- © 1967 by The Williams & Wilkins Company
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