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DIFFERENTIAL ROLES OF RYANODINE‐ AND THAPSIGARGIN‐SENSITIVE INTRACELLULAR Ca 2+ STORES IN EXCITATION–CONTRACTION COUPLING IN SMOOTH MUSCLE OF GUINEA‐PIG TAENIA CAECI
Author(s) -
Hishinuma Shigeru,
Saito Masaki
Publication year - 2006
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.1440-1681.2006.04506.x
Subject(s) - ryanodine receptor , thapsigargin , medicine , contraction (grammar) , carbachol , endocrinology , muscle contraction , chemistry , biophysics , intracellular , histamine , extracellular , biology , stimulation , biochemistry
SUMMARY1 To explore roles of intracellular Ca 2+ stores in excitation–contraction coupling in smooth muscle, we examined the effects of ryanodine, a fixer of ryanodine receptor–Ca 2+ channels to an open state, and thapsigargin, a selective inhibitor of the Ca 2+ pump in the intracellular stores, on smooth muscle contraction in the presence and absence of extracellular Ca 2+ in guinea‐pig taenia caeci. 2 In Ca 2+ ‐free solution, contractions induced by 0.1 mmol/L carbachol and 0.1 mmol/L histamine were reduced to approximately 65% of control by either 1 µmol/L thapsigargin or 10 µmol/L ryanodine. In contrast, caffeine‐induced contraction was reduced to approximately 40% of control by ryanodine, but was not affected by thapsigargin. 3 In the presence of extracellular Ca 2+ , thapsigargin slowly induced a large and sustained contraction. In contrast, ryanodine did not induce an apparent contraction, but increased the sensitivity of contractile responses to receptor agonists (carbachol, AHR‐602 and histamine) or depolarizing high K + with no changes in the maximal contraction. 4 These results suggest that there are pharmacological and physiological differences between ryanodine‐ and thapsigargin‐sensitive intracellular Ca 2+ stores in excitation–contraction coupling in smooth muscle, which may be responsible for their differential effects on the Ca 2+ ‐influx pathway.