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Involvement of purinergic nerves in the NANC inhibitory junction potentials in pigeon oesophageal smooth muscle

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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 m) and guanethidine (1 m), elicited an inhibitory response consisting of a transient hyperpolarization (inhibitory junction potential, IJP) associated with muscle relaxation.

2 Sodium nitroprusside (SNP, 100 m) induced hyperpolarization correlated to mechanical relaxation.

3 The nitric oxide (NO) synthase inhibitor N-nitro-l-arginine (from 0.1 to 100 m) caused a concentration-dependent reduction of electromechanical response to EFS indicating a role for NO in this response.

4 Apamin (1 m) 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 mto 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 m) 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.
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Keywords: IJP; NANC pathways; electrical field stimulation; oesophageal smooth muscle; pigeon; purines

Document Type: Research Article

Affiliations: 1: Dipartimento di Biologia cellulare e dello sviluppo, Laboratorio di Fisiologia, Università degli Studi di Palermo, Viale delle Scienze Parco d'Orleans II 90128 Palermo 2: Dipartimento di medicina sperimentale, Università di Palermo, Corso Tukory, 129, 90134 Palermo, Italy

Publication date: 2004-01-01

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