Abstract

Pupillary changes of isolated intact cat irides were investigated in vitro. Normal irides reacted to nicotine with miosis followed by mydriasis, but no changes in pupillary size occurred when the nicotine injection was repeated within 2 hr. The miotic phase of the effect of nicotine was due to a cholinergic mechanism, since it was abolished by atropine and was prolonged in physostigmine-treated irides. These findings, with observations that nicotine produced contraction followed by relaxation in cat iris sphincters and contraction in cat iris dilators, led to the conclusion that nicotine-induced miosis was due to sphincter contraction. Chronically parasympathetically denervated irides reacted to nicotine with mydriasis, while chronically sympathetically denervated irides reacted with miosis. These findings further support the earlier conclusion that nicotine-induced sphincter contraction resulted from postganglionic stimulation of parasympathetic nerve fibers. Treatment with hexamethonium revealed differences between the parasympathomimetic effects of nicotine and those of electrical parasympathetic stimulation. Hexamethonium-treated irides reacted after a long latency with protracted miosis, but showed unchanged electrically induced responses.