title: Parasympathetic depression of vas deferens contraction in the guinea-pig involves adenosine receptors.
abstract: 1. In the guinea-pig pelvic plexus-vas deferens preparation, stimulation of the parasympathetic pelvic nerves contracted the vas deferens then depressed the contractile responses to stimulation of the sympathetic hypogastric nerves. 2. The contraction caused by stimulation of the pelvic nerves was initially phasic then tonic. The contractions were almost abolished by application of hexamethonium to the plexus. The phasic contraction was abolished by alpha,beta-methylene adenosine triphosphate applied to the vas deferens. 3. Conditioning stimulation of the pelvic nerves preferentially depressed the phasic component of test contractions evoked by hypogastric nerve stimulation but did not affect the compound action potentials in postganglionic nerves evoked by test stimulation. 4. When the pelvic plexus was divided into two parts, one with the pelvic nerves and the other with the hypogastric nerves, conditioning stimulation of the pelvic nerves still depressed test contractions evoked by hypogastric nerve stimulation. 5. In the de-ganglionated vas deferens preparation, conditioning stimulation of some postganglionic nerves also depressed contractions evoked by test stimulation of the other postganglionic nerves. 6. 8-Phenyltheophylline (5-20 microM) applied to the vas deferens antagonized the conditioning stimulation-induced depression in both the pelvic plexus-vas deferens and the de-ganglionated preparations. 7. N6-Cyclohexyladenosine (CHA) and N6-(L-2-phenylisopropyl)-adenosine at 0.5 microM preferentially inhibited phasic contractions evoked by the postganglionic nerve stimulation. The effect of CHA was antagonized by 8-phenyltheophylline (10 microM). 8. The results indicate that the mechanism underlying the conditioning stimulation-induced depression of phasic contractions operates not in the ganglia, but through activation of adenosine receptors in the vas deferens.
authors.affiliation: Pharmacology Division, Meiji Institute of Health Science, Odawara, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Kurokawa
authors.forename: A
authors.initials: A
authors.lastname: Tsunoo
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000241:Adenosine / Q000031:analogs & derivatives / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D010275:Parasympathetic Nervous System / Q000502:physiology*; D010388:Pelvis / Q000294:innervation*; D011983:Receptors, Purinergic / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology; D013806:Theophylline / Q000031:analogs & derivatives / Q000494:pharmacology; D013997:Time Factors; D014649:Vas Deferens / Q000502:physiology*
chemical_list: D011983:Receptors, Purinergic; C027513:N(6)-cyclohexyladenosine; D000255:Adenosine Triphosphate; D013806:Theophylline; C028322:8-phenyltheophylline; D000241:Adenosine; C002630:alpha,beta-methyleneadenosine 5'-triphosphate