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K + ‐stimulation of the phosphoinositide pathway in guinea‐pig ileum longitudinal smooth muscle is predominantly neuronal in origin and mediated by the entry of extracellular Ca 2+
Author(s) -
Watson Stephen P.,
Lai Jeremy,
Sasaguri Toshiyuki
Publication year - 1990
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.1476-5381.1990.tb14681.x
Subject(s) - tetrodotoxin , extracellular , inositol , inositol phosphate , chemistry , stimulation , inositol trisphosphate , collagenase , carbachol , nifedipine , medicine , biophysics , biology , endocrinology , calcium , biochemistry , receptor , enzyme
1 K + and scorpion toxin stimulate formation of inositol phosphates in guinea‐pig ileum longitudinal smooth muscle slices. The response to these two agents is not additive. 2 The response to K + is inhibited partially by nifedipine and partially by ω‐conotoxin. When given together the effect of these two Ca 2+ channel blockers is additive and the response to K + is reduced by more than 80%. 3 The response to scorpion toxin is inhibited completely by tetrodotoxin, partially by ω‐conotoxin but not by atropine or nifedipine. Scorpion toxin induces a similar formation of inositol phosphates in collagenase‐dispersed cells to that seen in cross‐chopped slices. 4 The responses to scorpion toxin and K + are inhibited completely when the extracellular Ca 2+ concentration is reduced to below cytosolic levels (< 100 n m ). 5 Neither nifedipine nor ω‐conotoxin, either alone or in combination, inhibited formation of inositol phosphates by substance P or carbachol. Both of these agonists induced a significant formation of inositol phosphates even when the extracellular Ca 2+ concentration was reduced to 10 n m . 6 These results indicate that K + and scorpion toxin induce formation of inositol phosphates through the mobilisation of extracellular Ca 2+ . The response to K + appears to occur predominantly in neuronal cells.