Abstract

Relaxations of the isolated bovine retractor penis muscle elicited by nicotine and the three other nicotinic agonists acetylcholine, carbachol, and dimethylphenylpiperazinium were studied. Nicotine (10-45 microM) induced dose-dependent relaxations that closely resembled those evoked by transmural stimulation of inhibitory nerves. The relaxations induced by this dose level of nicotine were abruptly abolished by hypoxia and totally blocked by 1.2 microM mecamylamine, 45 microM lidocaine, and 13 microM methylene blue. They were reduced 50-90% by 0.16 microM tetrodotoxin, but they were unaffected by 17 microM scopolamine. Provided that sufficient concentrations of scopolamine and eserine were present, the relaxations caused by acetylcholine (30-140 microM) were exactly like those evoked by nicotine, and they were identically affected by hypoxia and the blocking drugs. Also carbachol and dimethylphenylpiperazinium induced relaxations qualitatively identical to those effected by the above-mentioned doses of nicotine. Relaxations induced by larger doses of nicotine were less susceptible to hypoxia and the blocking drugs. The results suggest that nicotine concentrations ranging from about 10-45 microM relax the bovine retractor penis muscle by a rather selective activation of inhibitory nerves, whereas higher concentrations may additionally activate some other less specific inhibitory mechanism. They further strongly suggest the presence of nerve cell bodies in this muscle. It is suggested that one physiological role of acetylcholine in the development of penile erection is nicotinic activation of inhibitory nerves. Moreover, nicotinic activation of these nerves of the bovine retractor penis muscle can be used as a model for further characterization of mammalian erectile nerves.