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Volume regulation in mammalian skeletal muscle: the role of sodium–potassium–chloride cotransporters during exposure to hypertonic solutions
Author(s) -
Lindinger Michael I.,
Leung Matthew,
Trajcevski Karin E.,
Hawke Thomas J.
Publication year - 2011
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 - 10.1113/jphysiol.2011.206730
Subject(s) - osmotic concentration , extracellular , chemistry , bumetanide , cotransporter , tonicity , skeletal muscle , sodium , biophysics , intracellular , ouabain , potassium , medicine , biochemistry , endocrinology , biology , organic chemistry
Non‐technical summary During moderate to high intensity exercise, there is a net flux of solute‐poor fluid into contracting skeletal muscle. This raises plasma osmolarity, and non‐contracting skeletal muscle and other tissues lose water to the vascular compartment to help maintain blood volume. The loss of water from these non‐contracting tissues causes the cells to shrink. For many tissues the shrinkage of the cells activates the sodium–potassium–chloride cotransporter (NKCC) which is situated in the plasma membrane. Activation of the NKCC reduces the volume loss and functions to restore cell volume in order to prevent cell damage and maintain cellular function. We show that this is also the case for mammalian skeletal myocytes and that the necessary sodium and chloride gradients to maintain NKCC activity depend on the continued activity of the sodium pump (Na + ,K + ‐ATPase).