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ROLE OF Ca 2+ STORES IN ACETYLCHOLINE‐INDUCED ALL‐OR‐NONE SHORTENING OF SMOOTH MUSCLE CELLS FROM GUINEA‐PIG TAENIA CAECUM
Author(s) -
Mita Mitsuo,
ToguchiSenrui Natsuko
Publication year - 2008
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2008.04917.x
Subject(s) - cyclopiazonic acid , taenia coli , egta , acetylcholine , caecum , guinea pig , intracellular , inositol , endocrinology , medicine , biology , calcium , endoplasmic reticulum , muscle contraction , biochemistry , chemistry , receptor
SUMMARY1 We have reported previously that isolated single smooth muscle cells from guinea‐pig taenia caecum respond to acetylcholine (ACh) in an all‐or‐none manner. 2 To clarify the roles of intracellular Ca 2+ stores in the all‐or‐none response of isolated smooth muscle cells from guinea‐pig taenia caecum to ACh, we examined the inositol 1,4,5‐trisphosphate (IP 3 )‐induced contractile response in Staphylococcus aureus a‐toxin‐permeabilized smooth muscle cells and the effect of depletion of intracellular Ca 2+ stores on the all‐or‐none response to ACh in intact smooth muscle cells. 3 a‐Toxin‐permeabilized smooth muscle cells responded to 3–30 nmol/L or 0.3–3 nmol/L IP 3 in the presence of 0.2 mmol/L Ca 2+ with 1 mmol/L EGTA or 0.1 mmol/L EGTA, respectively, in an all‐or‐none manner. These results suggest that Ca 2+ release induced by IP 3 is Ca 2+ dependent and is evoked in an all‐or‐none manner. 4 In the presence of the Ca 2+ ionophore A23187 (0.1 mmol/L) or the sarcoplasmic reticulum Ca 2+ ‐ATPase inhibitor cyclopiazonic acid (1 mmol/L), the shortening of intact smooth muscle cells induced by increasing concentrations of ACh showed a graded response, but not an all‐or‐none response. 5 In conclusion, the results suggest that Ca 2+ release from Ca 2+ stores induced by IP 3 plays an important role in the all‐or‐none response of intact smooth muscle cells to ACh.