title: Evidence for a role for nitric oxide in relation of the frog oesophageal body to electrical field stimulation.
abstract: 1. Electrical field stimulation (EFS) (1-10 Hz, 30 V, 2 ms) of frog oesophageal body strips resulted in frequency-dependent non-adrenergic, non-cholinergic (NANC) relaxations. 2. Tetrodotoxin (TTX) (10(-6)-10(-5) M) had no effect on EFS evoked relaxations with a 2 ms pulse width. At a pulse width of 0.5 ms only the responses to the highest frequency (10 Hz) were significantly inhibited by TTX at 10(-5) M. Relaxation at 2 ms pulse width were unaffected by omega-conotoxin (10(-6) M), nifedipine (10(-6) M) or cobalt (5 x 10(-4) M). 3. NG-nitro-L-arginine (L-NOARG) (10(-6)-10(-4) M), a nitric oxide synthase (NOS) inhibitor, caused a concentration-dependent inhibition of the EFS-induced NANC relaxant responses. The inhibitory effect of L-NOARG was both prevented and reversed by L-arginine but not D-arginine (5 x 10(-3) M). 4. The phosphodiester type V inhibitor (PDE V), SK&F 96231 (10(-7)-10(-4) M), caused a concentration-dependent potentiation of both the percentage relaxation and the duration of the relaxant responses to EFS. 5. ODQ (10(-7)-10(-5) M), a guanylate cyclase inhibitor, produced a concentration-dependent inhibition of EFS-evoked NANC relaxations. 6. Oxyhaemoglobin (10(-6) M), which binds nitric oxide (NO), inhibited NANC relaxations to EFS. 7. The NO donor sodium nitroprusside (SNP) (10(-8)-10(-4) M) produced a concentration-dependent inhibition of evoked tone. L-NOARG (10(-4) M) had no effect on the SNP evoked relaxations. Preincubation with oxyhaemoglobin (10(-6) M) caused a reduction in the SNP (10(-6)-10(-5) M) induced relaxations. 8. These results suggest NO is the relaxant transmitter of the frog oesophageal body and the source of NO may be non-neuronal.
authors.affiliation: Biosciences Division, University of Hertfordshire.
authors.forename: S J
authors.initials: SJ
authors.lastname: Williams
authors.forename: M E
authors.initials: ME
authors.lastname: Parsons
mesh_terms: D018663:Adrenergic Agents / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004947:Esophagus / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D005260:Female; D006145:Guanethidine / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009126:Muscle Relaxation / Q000187:drug effects / Q000502:physiology*; D009130:Muscle, Smooth / Q000187:drug effects / Q000294:innervation / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology*; D019335:Nitroarginine / Q000494:pharmacology; D010528:Peristalsis / Q000187:drug effects / Q000502:physiology; D011898:Ranidae; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D018663:Adrenergic Agents; D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D019335:Nitroarginine; D009569:Nitric Oxide; D013779:Tetrodotoxin; D002217:Carbachol; D001120:Arginine; D007213:Indomethacin; D006145:Guanethidine