Parasympathetic innervation of rat peri-orbital smooth muscle: prejunctional cholinergic inhibition of sympathetic neurotransmission without direct postjunctional actions.

The role of parasympathetic neurotransmission in regulating periorbital smooth muscle function was investigated in urethane-anesthetized rats. Parasympathetic nerves were activated by stereotaxic electrical stimulation (20 Hz, < or = 2.0 V) of the ipsilateral superior salivatory nucleus, which gives rise to preganglionic innervation to the pterygopalatine ganglion and hence to the orbital targets. This approach permits selective parasympathetic activation that cannot be attained at more peripheral sites. Target responses were measured by recording changes in tarsal smooth muscle tension from the superior eyelid. Parasympathetic stimulation caused a small decrease in resting tension (-73 +/- 4 mg) that was not altered when the muscle was partially contracted with methoxamine. However, adrenoceptor-mediated contraction induced by cervical sympathetic nerve stimulation was attenuated in a frequency-dependent manner, with inhibition greatest at higher sympathetic stimulation frequencies (-338 +/- 35 mg at 8 Hz). This attenuation was blocked by the muscarinic receptor antagonist atropine methyl nitrate. Administration of the muscarinic agonist bethanechol increased resting tarsal muscle tension (655 +/- 34 mg). However, sympathetically mediated contraction at 2 Hz (1295 +/- 53 mg) was decreased by bethanechol administration to a value (710 +/- 37 mg) not significantly different from the contraction caused by bethanechol alone. We conclude that muscarinic receptors are present on tarsal smooth muscle, where they elicit contractions, and on sympathetic nerves, where they inhibit neurotransmission presumably by depressing noradrenaline release.(ABSTRACT TRUNCATED AT 250 WORDS)