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Part of the book series: Physiology in Health and Disease ((PIHD))

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Abstract

Large, Ca2+-activated K+ channels (BK) are comprised of the pore-forming α subunit (BK-α) and one of four β subunits (β1–4), which bestows functional diversity. BK channels are localized in the distal nephron of kidneys and a variety of extrarenal, fluid-secreting epithelia. In the kidneys, flow activates BK, which are located in two cell types of the distal nephron. The BK-α/β1 resides in the connecting tubule cells, and the BK-α/β4 is localized in intercalated cells, where they mediate K+ secretion in mice on a high K+, alkaline diet.

BK channels mediate K+ secretion from goblet cells of the colon to generate fluid volume, as part of a neurogenic-stimulated response to infection or bacterial imbalance. In the ductal cells of the exocrine glands and pancreas, BK mediate K+ secretion in conjunction with HCO3 to generate an alkaline volume in order to neutralize the acidic contents of the mouth and stomach. In pulmonary epithelia, BK mediate secretion of K+, as a counter cation to Cl, to drive secretion of fluid volume.

BK also reside in the basolateral membranes of some epithelial cells, where they have a role to drive Cl secretion or Na+ absorption by serving to recycle cellular K+ that entered via Na+-K+-ATPase. In summary, BK-mediated K+ secretion, which contributes to K+ homeostasis in response to aldosterone in renal distal tubules and colon, serves to drive high volumes of fluid in response to muscarinic and/or adrenergic stimulation in the colon and other extrarenal epithelia.

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Correspondence to Steven C. Sansom .

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Wen, D., Cornelius, R.J., Sansom, S.C. (2016). BK Channels in Epithelia. In: Hamilton, K., Devor, D. (eds) Ion Channels and Transporters of Epithelia in Health and Disease. Physiology in Health and Disease. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-3366-2_21

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