No abstract

Pigeon oesophageal smooth muscle in vitro has spontaneous electromechanical activity. In the presence of atropine and guanethidine, electrical field stimulation evokes a transient TTX-sensitive response comprising inhibition of electric bursting activity and muscular relaxation. This NANC inhibitory response was analysed using the K+ channel blockers TEA and apamin, TEA perfusion (0.1-5 mM) induced a concentration-dependent reduction in amplitude of EFS-evoked relaxation. Responses to higher stimulation frequencies were more sensitive to TEA than those to lower ones. The maximum reduction in amplitude (29% of control) was obtained on 30 Hz EFS evoked responses during 5 mM TEA perfusion. In a similar way, apamin (0.01-10 microM) perfusion reduced NANC relaxation, up to 30% of control. These results suggest that in the pigeon oesophagus, NANC intramural neurons are responsible for muscular relaxation. We speculate that an increase in K+ conductance might be the main mechanism involved, although the residual response after K+ channel blockade indicates the existence of an additional ionic mechanism.

The effects of the efferent glossopharyngeal nerve stimulation, on EMG activity of the pigeon cervical oesophagus, were studied. In control animals, stimulation caused a biphasic response characterized by an intra-stimulus excitatory component followed by a post-stimulus inhibitory one. The EMG response to glossopharyngeal stimulation appeared simultaneously throughout the cervical oesophagus. A bell-shaped mechanical wave was detected relating to the electrical excitatory component. Atropine administration antagonized the excitatory component, while the inhibitory one persisted. It occurs intra-stimulus, and its duration is increased, compared to control ones. A reduction in the oesophageal resting pressure was observed relating to the electrical inhibitory component. Hexamethonium caused complete disappearance of any EMG response to glossopharyngeal stimulation, as well as suppression of mechanical responses. The comparison between the EMG responses to swallow and to efferent glossopharyngeal stimulation suggests that in pigeon cervical oesophagus: primary peristalsis is central in origin; a dual system of glossopharyngeal fibres, excitatory and inhibitory, carries the central control for oesophageal motility; these excitatory and inhibitory fibres supply the oesophageal muscle via intramural neurons; the synaptic arrangement of the inhibitory pathway is more complex than the excitatory one.

Swallowing elicits two propagated EMG peristaltic patterns in pigeon cervical oesophagus: i) "simple" peristaltic pattern and ii) "complex" peristaltic pattern. "Simple" peristaltic pattern is characterized by an intense, long-lasting burst of spikes, high in amplitude with an aboral increasing delay in onset. "Complex" peristaltic pattern presents an early short period of reduction in spontaneous electrical activity, followed by an excitatory period similar to that of "simple" pattern. The early inhibitory component has a very short delay in onset increasing aborally. Atropine abolishes the EMG excitatory component of both patterns, while the inhibitory period persists, showing increased duration and reduced propagation speed. "Simple" peristaltic pattern, mediated by cholinergic nerves, acting on muscular muscarinic receptors, is identifiable with an "on response". "Complex" peristaltic pattern shows a cholinergic muscarinic excitatory component and an atropine-resistant inhibitory component. This latter component is not a passive post-inhibitory rebound ("off response").

1. Electrical field stimulation (EFS) (0.5 ms in train of 2-32 Hz for 300 ms) in smooth muscle of pigeon oesophagus, in the presence of atropine (1 microm) and guanethidine (1 microm), elicited an inhibitory response consisting of a transient hyperpolarization (inhibitory junction potential, IJP) associated with muscle relaxation. 2. Sodium nitroprusside (SNP, 100 microm) induced hyperpolarization correlated to mechanical relaxation. 3. The nitric oxide (NO) synthase inhibitor N(omega)-nitro-l-arginine (from 0.1 to 100 microm) caused a concentration-dependent reduction of electromechanical response to EFS indicating a role for NO in this response. 4. Apamin (1 microm) reduced both IJP and relaxation to EFS but was without effect on the response to SNP indicating a role for purines, which are also blocked by apamin. 5. Adenosine, AMP, ADP and ATP (all from 1 microm to 1 mm) application caused transient hyperpolarization and muscular relaxation with the following order of potency: adenosine > AMP > ADP > ATP. 6. Inhibitory responses evoked by purines are TTX (1 microm) insensitive but they were inhibited by apamin. This indicates that a purine component for the non-adrenergic non-cholinergic (NANC) response exists but the purine receptor site is not located on the neurone. 7. Overall these results suggest that NANC inhibitory response elicited by EFS presents two different components apamin-sensitive, probably purines-mediated and apamin-insensitive probably NO-mediated as apamin only partially block the response to EFS.