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Department of Physiology, University of Geneva, Centre Medical Universitaire, Switzerland.

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.

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