ADRENERGIC MECHANISMS IN THE RELAXATION OF GUINEA-PIG TAENIA COLI IN VITRO

¹ Department of Pharmacology, The University of Michigan Medical School and Department of Pharmacology, Divsion of Medical and Scientific Affairs, Parke, Davis and Company, Ann Arbor, Michigan

Relaxation of taenia contracted in 35 mM K⁺ media was induced by electrical field stimulation and by the addition of nicotine. The responses to field stimulation and to nicotine were dependent on the intensity and frequency of the electrical stimulus or the concentration of nicotine; the responses to both were inhibited competitively by tolasoline. Relaxation to either stimulus was reduced by phentolamine, propranolol or lidocaine and was abolished by tetrodotoxin. In the presence of hexamethonium or nicotine the relaxation to nicotine was prevented but that to field stimulation was unaffected. Guanethidine, in doses which abolished responses to perivascular nerve stimulation (see below), partially reduced relaxation to field stimulation. Phentolamine and guanethidine were additive in their inhibition of relaxation to field stimulation. Axonal stimulation of the perivascular nerves elicited relaxation of taenia in 5.9 mM K⁺ media but not in media containing 35 mM K⁺. In 5.9 mM K⁺ media, the taenia recovered from the relaxant effects of field stimulation immediately upon cessation of stimulation, whereas the relaxation induced by stimulation of perivascular nerves persisted for 10 to 20 seconds after the stimulus was terminated. In the presence of cocaine, the relaxant effects of both forms of stimulation were greatly prolonged. It is our hypothesis that both nicotine and electrical stimulation produced relaxation of guinea-pig taenia coli by releasing catecholamines from adrenergic nerves. Field stimulation excites adrenergic nerves which terminate on smooth muscle cells. Perivascular nerve stimulation releases catecholarnines from nerves which terminate on the excitatory ganglion cells of Auerbach's plexus.