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Multiple pathways responsible for the stretch‐induced increase in Ca 2+ concentration in toad stomach smooth muscle cells
Author(s) -
Kirber Michael T.,
GuerreroHernández Agustín,
Bowman Douglas S.,
Fogarty Kevin E.,
Tuft Richard A.,
Singer Joshua J.,
Fay Fredric S.
Publication year - 2000
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2000.t01-4-00003.x
Subject(s) - pipette , depolarization , biophysics , membrane potential , chemistry , ryanodine receptor , intracellular , ion channel , patch clamp , toad , membrane , calcium , reversal potential , biochemistry , biology , receptor , endocrinology , organic chemistry
1 A digital imaging microscope with fura‐2 as the Ca 2+ indicator was used to determine the sources for the rise in intracellular calcium concentration ([Ca 2+ ] i ) that occurs when the membrane in a cell‐attached patch is stretched. Unitary ionic currents from stretch‐activated channels and [Ca 2+ ] i images were recorded simultaneously. 2 When suction was applied to the patch pipette to stretch a patch of membrane, Ca 2+ ‐permeable cation channels (stretch‐activated channels) opened and a global increase in [Ca 2+ ] i occurred, as well as a greater focal increase in the vicinity of the patch pipette. The global changes in [Ca 2+ ] i occurred only when stretch‐activated currents were sufficient to cause membrane depolarization, as indicated by the reduction in amplitude of the unitary currents. 3 When Ca 2+ was present only in the pipette solution, just the focal change in [Ca 2+ ] i was obtained. This focal change was not seen when the contribution from Ca 2+ stores was eliminated using caffeine and ryanodine. 4 These results suggest that the opening of stretch‐activated channels allows ions, including Ca 2+ , to enter the cell. The entry of positive charge triggers the influx of Ca 2+ into the cell by causing membrane depolarization, which presumably activates voltage‐gated Ca 2+ channels. The entry of Ca 2+ through stretch‐activated channels is also amplified by Ca 2+ release from internal stores. This amplification appears to be greater than that obtained by activation of whole‐cell Ca 2+ currents. These multiple pathways whereby membrane stretch causes a rise in [Ca 2+ ] i may play a role in stretch‐induced contraction, which is a characteristic of many smooth muscle tissues.

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