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Critical intracellular Ca2+ concentration for all‐or‐none Ca2+ spiking in single smooth muscle cells.
Author(s) -
Iino M.,
Yamazawa T.,
Miyashita Y.,
Endo M.,
Kasai H.
Publication year - 1993
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1993.tb06224.x
Subject(s) - biology , intracellular , biophysics , myocyte , microbiology and biotechnology
Neurotransmitters induce contractions of smooth muscle cells initially by mobilizing Ca2+ from intracellular Ca2+ stores through inositol 1,4,5‐trisphosphate (InsP3) receptors. Here we studied roles of the molecules involved in Ca2+ mobilization in single smooth muscle cells. A slow rise in cytoplasmic Ca2+ ([Ca2+]i) in agonist‐stimulated smooth muscle cells was followed by a wave of rapid regenerative Ca2+ release as the local [Ca2+]i reached a critical concentration of approximately 160 nM. Neither feedback regulation of phospholipase C nor caffeine‐sensitive Ca(2+)‐induced Ca2+ release was found to be required in the regenerative Ca2+ release. These results indicate that Ca(2+)‐dependent feedback control of InsP3‐induced Ca2+ release plays a dominant role in the generation of the regenerative Ca2+ release. The resulting Ca2+ release in a whole cell was an all‐or‐none event, i.e. constant peak [Ca2+]i was attained with agonist concentrations above the threshold value. This finding suggests a possible digital mode involved in the neural control of smooth muscle contraction.

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