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Role of sarcoplasmic reticulum in inhibitory junction potentials and hyperpolarizations by nitric oxide donors in opossum oesophagus
Author(s) -
Cayabyab Francisco S.,
Daniel Edwin E.
Publication year - 1996
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1996.tb15661.x
Subject(s) - cyclopiazonic acid , chemistry , biophysics , endoplasmic reticulum , nitric oxide , inhibitory postsynaptic potential , ryanodine receptor , depolarization , tetraethylammonium , ouabain , hyperpolarization (physics) , biochemistry , endocrinology , stereochemistry , biology , sodium , potassium , organic chemistry , nuclear magnetic resonance spectroscopy
1 Previous patch clamp studies of oesophageal circular muscle cells showed that nitric oxide (NO) modulated the opening of Ca 2+ ‐activated K + channels involved in mediating the inhibitory junction potentials (i.j.ps). This study clarified the role of Ca 2+ 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 μ m , hyperpolarized oesophageal circular muscle cells by 15–20 mV, like i.j.ps. 3 The selective inhibitors of SR Ca 2+ ‐ATPase (cyclopiazonic acid 10–30 μ m and thapsigargin 5 μ m ) and the SR Ca 2+ release channel activator (ryanodine 30 μ m ) caused depolarization and spontaneous contractions which were diminished after prolonged (>30 min) incubation with these agents in Ca 2+ ‐containing medium. Moreover, these agents inhibited both the i.j.p. and NO‐donor hyperpolarizations, suggesting that a functional SR Ca 2+ 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 Ca i 2+ elevation, via vectorial Ca 2+ 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.