NEUROGENIC BASIS FOR THE RISE IN BLOOD PRESSURE EVOKED BY NICOTINE IN THE CAT

¹ Department of Pharmacology, Michigan State University, East Lansing, Michigan

The pressor response elicited by small i.v. doses of nicotine (5-40 µg/kg) was accompanied by an increase in centrally emanating nerve activity recorded from both pre- and postganglionic branches of the superior cervical ganglion. The presser response was abolished by transection of the spinal cord and was somewhat reduced after denervation of the aortic and carotid body chemoreceptors. Nicotine-induced enhancement of postganglionic activity recorded from the innervated ganglion also was somewhat reduced after chemoreceptor denervation. However, chemoreceptor denervation abolished the enhancement of centrally emanating preganglionic activity produced by nicotine. Although the doses of nicotine employed were too small to evoke a postganglionic discharge in the decentralized ganglion, they were sufficient to facilitate the postganglionic action potential evoked by submaximal stimulation of the sectioned preganglionic nerve. It is concluded that the major component of the pressor response produced by small i.v. doses of nicotine is the consequence of facilitation of ganglionic transmission rather than a direct central effect of the compound on vasomotor areas. This study also illustrates that abolition of an autonomic neuroeffector response by spinal cord section does not necessarily indicate that the response was of supraspinal origin.

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