Abstract

Effects of nicotine on gastrointestinal contractile activity monitored by acutely implanted extraluminal strain gauge force transducers were dotermined in pentobarbital-anesthetized dogs. Close i.a. infusions of nicotine, 5 to 25 µg/kg/min, produced an initial stimulation followed by inhibition of contractile activity of both the gastric antrum and duodenum. In contrast, the i.v. administration of nicotine, 100 µg/kg, produced an initial inhibition of activity followed by a period of stimulation. The inhibition induced by the i.v. administration of nicotine was decreased by adrenalectomy (38%), vagotomy combined with splanchnicotomy (26%) and vagotomy combined with spinal anesthesia (49%). The secondary stimulation induced by the i.v. administration of nicotine was abolished by adrenalectomy. Inhibition of contractile activity by i.v. administered nicotine was attributed to activation of adrenergic systems. Catecholamine release was due in part to actions of nicotine on afferent neuronal or central nervous system structures and the adrenal glands. Indirect evidence suggested that the remainder of the release of catecholamines may be due to a stimulation of sympathetic ganglia. Adrenergic mediators released by nicotine appeared to act on neuronal elements rather than directly on smooth muscle since nicotine inhibited vagal-stimulated but not methacholine-induced contractile activity.