Characterization of bumetanide-sensitive Na+ and K+ transport in rat skeletal muscle

In isolated rat soleus muscle an average of 23% of the total Na-22 influx was found to be suppressible by bumetanide (K-0.5 = 0.1 mM) and furosemide (K-0.5 = 1 mM), whereas the influx and efflux oi K-42 were not affected. In extensor digitorum longus muscle, around 25% of the total Na-22 influx was suppressible by bumetanide (1 mM). in the presence of ouabain, both diuretics decreased net intracellular accumulation oi Na+, but caused no change in K+ content. In extensor digitorum longus (but not in soleus), bumetanide-suppressible Na-22 influx was stimulated by increasing extracellular osmolarity with the bumetanide having no effect on K-42 influx. Bumetanide-suppressible Na+ influx was almost abolished in Cl--free buffer, but was unaffected by the omission of K+. in rat soleus. the inhibitory effects of bumetanide, amiloride and tetrodotoxin on Na-22 influx were found to be additive. The results indicate that a NaCl cotransport system is present in both fast- and slow-twitch skeletal muscles. and may participate in volume regulation. Due to the large pool of muscle cells, activation oi NaKCl2 cotransport is likely to entail the hazards oi hypokalemia. The advantage of exerting volume control via NaCl cotransport is that this risk can be avoided.