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1 Copenhagen Muscle Research Centre, Institute of Molecular Biology and Physiology, Copenhagen, DK-2100, Denmark
2 Department of Epidemiology and Biostatistics, National Institute of Public Health, Copenhagen, DK-2100, Denmark
* To whom correspondence should be addressed. E-mail: mkristensen{at}aki.ku.dk.
Muscle activity is associated with potassium displacements, which may cause fatigue. It has previously been reported that the density of the Big Conductance Ca2+-dependent K+ (BKCa2+) channel is higher in the T-tubule membrane than in the sarcolemmal membrane and that the opposite is the case for the ATP-sensitive K+ (KATP) channel. In the present experiment we investigated the subcellular localizations of the strong inward rectifier 2.1 K+ (Kir2.1) channel and the Na+, K+, 2Cl- 1 (NKCC1) co-transporter using western blotting of different muscle fractions. Furthermore muscle function was studied when trying to manipulate the opening probability or transport capacity of these proteins during electrical stimulation of isolated soleus muscles. All experiments were made with excised muscle from male Wistar rats. The Kir2.1 channels were almost undetectable in the sarcolemmal membrane but present in the T-tubule membrane, whereas the NKCC1 co-transporters were present in the sarcolemmal membrane. For muscles incubated in a buffer containing either Pinacidil, NS1619, Ba2+, or bumetanide there was a faster reduction in peak force (P < 0.05). Furthermore, bumetanide incubation reduced the peak force at the onset of electrical stimulation (P < 0.05). Thus, the effects on muscle force indicate that these drugs can affect K+ transporting proteins and thereby influence K+ accumulation especially in the T-tubules, suggesting that KATP and BKCa2+ channels are responsible for K+ release and decrease in force during repeated muscle contractions while Kir2.1 and NKCC1 may have a role in K+ reuptake.
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