Pharmacological and electrophysiological analysis of the effects of nicotine on cat blood pressure.

Nicotine (20-60 micrograms/kg) produced an initial vasodepressor response followed by a vasopressor response in anaesthetized cats, the mechanism of which was investigated. The vasodepressor response was antagonized by atropine or by vagotomy and was potentiated by physostigmine or neostigmine. Nicotine increased the single unit activity of different peripheral sympathetic nerves and evoked contraction of nictitating membrane and spleen along with vasopressor response. The vasopressor response was antagonized by phentolamine, prazosin, guanethidine, bretylium, 6-OHDA, hemicholinium-3 or hexamethonium. Propranolol or atenolol pretreatment potentiated the vasodepressor response and was antagonized by atropine. Desensitization by salbutamol did not modify the response to nicotine. The biphasic response to nicotine remained unaltered in yohimbine pretreated, in adrenalectomized, and in acute spinal as well as in decapitated animals; intracarotid or intracerebroventricular administration of nicotine did not produce any response. The biphasic response to nicotine does not involve the stimulation of the central vasomotor centre. In conclusion, these results suggest that the vasodepressor response is due to the vagal cholinergic mechanism. The vasopressor response is a consequence of activation of different peripheral adrenergic nerves causing increased release of the adrenergic transmitter at the neuroeffector region and the alpha 1-adrenoceptor mediate vasoconstriction in the systemic vascular bed.