Abstract
An investigation of some aspects of the pharmacological activity of (-)-cotinine, a metabolite of (-)-nicotine, has demonstrated that, in the anesthetized dog, (-)-cotinine lacks the potent pressor activity associated with the parent compound. In addition, it has been shown that (-)-cotinine has a depressor activity which was not abolished by ordinary blocking doses of atropine or diphenhydramine. The presence of depressor activity in the decerebrate and spinal dog is consistent with the suggestion that the effect may be mediated through the ability of (-)-cotinine to produce, directly or indirectly, a vascular muscular relaxation. The quantities of (-)-cotinine employed to produce the observed pharmacological effects were in excess of amounts which would arise in vivo from the metabolism of lethal or nonlethal doses of (-)-nicotine.
Footnotes
- Received April 30, 1962.
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