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Isoprenaline-stimulated differential adrenergic response of K+ channels in skeletal muscle under hypokalaemic conditions

  • Ion Channels, Transporters
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Abstract

The mechanism underlying the hyperpolarization induced by isoprenaline in mouse lumbrical muscle fibres was studied using cell-attached patch and intracellular membrane potential (V m) recordings. Sarcolemmal inwardly rectifying K+ channels (KIR: 45 pS) and Ca2+-activated K+ channels (BK: 181 pS) were identified. Exposure to isoprenaline closed KIR channels and increased BK channel activity. This increase was observed as a shift from 50 to −40 mV in the voltage dependence of channel activation. Isoprenaline prevented hysteresis of V m when the extracellular [K+] fell below 3.8 mM. This hysteresis was due to the properties of the KIR. The effects of chloride transport and isoprenaline on V m did not interact purely competitively, but isoprenaline could prevent the depolarization induced by hyperosmotic media equally as well as bumetanide, which inhibits the Na+/K+/2Cl cotransporter. In lumbrical muscle this leads to hyperpolarization, but this might vary among muscles. The switch from KIR to BK as the component of total K+ conductance was due to isoprenaline.

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Acknowledgements

We are grateful to the department of Physiology and Biophysics of the State University of New York at Buffalo, and to Lorin Milescu in particular, for the introduction to QuB. We are also grateful to Dr Gerard Borst for his advice and the use of the Sutter P-97 electrode puller, to Dr Wytse Wadman for his constructive remarks and to Dr Dirk Ypey for encouragement.

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Correspondence to J. Siegenbeek van Heukelom.

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Geukes Foppen, R.J., Siegenbeek van Heukelom, J. Isoprenaline-stimulated differential adrenergic response of K+ channels in skeletal muscle under hypokalaemic conditions. Pflugers Arch - Eur J Physiol 446, 239–247 (2003). https://doi.org/10.1007/s00424-003-1042-y

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  • DOI: https://doi.org/10.1007/s00424-003-1042-y

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