title: Role of sarcoplasmic reticulum in inhibitory junction potentials and hyperpolarizations by nitric oxide donors in opossum oesophagus.
abstract: 1. Previous patch clamp studies of oesophageal circular muscle cells showed that nitric oxide (NO) modulated the opening of Ca2(+)-activated K+ channels involved in mediating the inhibitory junction potentials (i.j.ps). This study clarified the role of Ca2+ release from the superficial sarcoplasmic reticulum (SR) in the mechanism of i.j.ps or hyperpolarizing responses to NO-releasing compounds. Electrical and mechanical activities were simultaneously recorded by intracellular microelectrode or double sucrose gap techniques. 2. The NO-donors, sydnonimine (SIN-1) and sodium nitroprusside, each at 500 microM, hyperpolarized oesophageal circular muscle cells by 15-20 mV, like i.j.ps. 3. The selective inhibitors of SR Ca2(+)-ATPase (cyclopiazonic acid 10-30 microM and thapsigargin 5 microM) and the SR Ca2+ release channel activator (ryanodine 30 microM) caused depolarization and spontaneous contractions which were diminished after prolonged (> 30 min) incubation with these agents in Ca2(+)-containing medium. Moreover, these agents inhibited both the i.j.p. and NO-donor hyperpolarizations, suggesting that a functional SR Ca2+ uptake is necessary for the response to endogenous or exogenous NO. 4. These results, along with our previous findings of the dependence of i.j.ps and NO-donor hyperpolarizations on K+ channel activation and cyclic GMP elevation, support the hypothesis that subplasmalemmal (Ca2+)i elevation, via vectorial Ca2+ release from superficial SR toward the plasmalemma, may be an important mechanism by which NO, from NO-liberating compounds or released from inhibitory neurones induces relaxation and i.j.ps in opossum oesophagus.
authors.affiliation: McMaster University, Department of Biomedical Sciences, Hamilton, Ontario, Canada.
authors.forename: F S
authors.initials: FS
authors.lastname: Cayabyab
authors.forename: E E
authors.initials: EE
authors.lastname: Daniel
mesh_terms: D000818:Animals; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D004947:Esophagus / Q000187:drug effects*; D005260:Female; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects*; D008981:Molsidomine / Q000031:analogs & derivatives* / Q000494:pharmacology; D009569:Nitric Oxide / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology; D009893:Opossums; D012519:Sarcoplasmic Reticulum / Q000187:drug effects*
chemical_list: D004791:Enzyme Inhibitors; D009599:Nitroprusside; D009569:Nitric Oxide; C002385:linsidomine; D008981:Molsidomine