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Ca(2+)‐dependent heat production by rat skeletal muscle in hypertonic media depends on Na(+)‐Cl‐ co‐transport stimulation.
Author(s) -
Chinet A
Publication year - 1993
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.1993.sp019536
Subject(s) - bumetanide , osmotic concentration , chemistry , stimulation , osmole , extracellular , sodium , endocrinology , medicine , cotransporter , tonicity , biophysics , ion transporter , dantrolene , biochemistry , calcium , biology , organic chemistry , membrane
1. The rate of energy dissipation (E) in isolated, superfused soleus muscles from young rats was continuously measured under normosmotic and 100‐mosM hyperosmotic conditions. The substantial increase of E with respect to basal level in hyperosmolarity (excess E), which is entirely dependent on the presence of extracellular sodium, was largely prevented or inhibited by bumetanide, a potent inhibitor of Na(+)‐Cl‐ co‐transport system, or by the removal of chloride from the superfusate (isethionate substitution). Bumetanide or the removal of chloride also acutely decreased basal E, by about 7%. 2. Bumetanide almost entirely suppressed the major, Ca(2+)‐dependent part of excess E in hyperosmolarity, as well as the concomitant increase of 45Ca2+ efflux and small increase in resting muscle tension; in contrast, the part of excess E associated with stimulation of Na(+)‐H+ exchange in hyperosmolarity was left unmodified. 3. Reduction of 22Na+ influx by bumetanide was more marked in hyperosmolarity than under control conditions, although stimulation of total 22Na+ influx by a 100‐mosM stress was not statistically significant. Inhibition of Ca2+ release into the sarcoplasm using dantrolene sodium did not prevent the stimulation of bumetanide‐sensitive 22Na+ influx, but rather increased it about fourfold. 4. It is concluded that the largest part of excess E in hyperosmolarity, which is Ca(2+)‐dependent energy expenditure, is suppressed when steady‐state stimulation of a Na(+)‐Cl‐ co‐transport system is inhibited either directly by bumetanide or the removal of extracellular chloride, or indirectly by the blocking of active Na(+)‐K+ transport. How the stimulation of Na(+)‐Cl‐ co‐transport, by as little as 1 nmol s‐1 (g wet muscle weight)‐1 during a 100‐mosM stress, enhances Ca(2+)‐dependent heat by as much as 2.5 mW (g wet muscle weight)‐1 remains to be clarified.