Effects of anisodine on respiratory center

Anisodine (Ani), a new selective M receptor blocking agent, was isolated from Scopolia tangutica in China. The structure of Ani is similar to scopolamine. Ani (2.5, 5 mg.kg-1 i.v., or 0.6 mg.kg-1 icv) increased the rate of phrenic nerve discharges (PND), while the time of inspiration and expiration, and the spikes in each PND were reduced in urethan-anesthetized rats. In urethan-anesthetized rabbits, Ani (2.5 mg.kg-1 i.v., or 0.2 mg.kg-1 applied onto obex) increased the rate of PND. In tubocurarine-pretreated and artificially ventilated rabbits, Ani (2.5 mg.kg-1 i.v., or 0.2 mg.kg-1 applied onto obex) increased the rate of inspiratory neurone firing in nucleus tractus solitarius. Oxotremorine (40 micrograms.kg-1 i.v.) antagonized the Ani effects. Ani (2.5 mg.kg-1 i.v.) partially antagonized the respiratory depression induced by morphine. These results provide the evidence that Ani stimulates the respiratory center through cholinergic M pathway and there may be some neuronal interaction between cholinergic and opiate receptors in the control of respiratory center.