Presence of a Ca2+-dependent K+ channel in brown adipocytes. Possible role in maintenance of alpha 1-adrenergic stimulation.
We have previously demonstrated mobilization of Ca2+ in and efflux of Rb+ (K+) from isolated hamster brown adipocytes as a consequence of norepinephrine stimulation. We have now investigated the adrenoceptor subtype specificity of these responses and found them both to be of the alpha 1-subtype. Further, we have found that the Rb+ (K+) efflux was dependent upon a primary Ca2+ mobilization event in response to the alpha 1-adrenergic stimulation, since the Rb+ efflux could also be demonstrated by the addition of the Ca2+ ionophore A23187 to the cells. The norepinephrine- and A23187-stimulated Rb+ effluxes were both inhibited by the Ca2+-dependent K+-channel blocker apamin. Apamin also significantly attenuated Ca2+ mobilization in cells in response to a submaximal concentration of norepinephrine. We conclude that alpha 1-adrenergic stimulation of brown fat cells leads to a mobilization of intracellular Ca2+ which, in itself or via other mechanisms, leads to an increase in cytosolic Ca2+ concentration which, in turn, activates a Ca2+-dependent K+ channel, leading to a K+ release from these cells. A possible role for this channel to sustain and augment the response to alpha 1-adrenergic stimulation is discussed.
Nånberg
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Connolly
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Nedergaard
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D002001:Adipose Tissue, Brown / Q000502:physiology*; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D006224:Cricetinae; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D008647:Mesocricetus; D009638:Norepinephrine / Q000494:pharmacology; D011188:Potassium / Q000502:physiology*; D011803:Quinine / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*
D007473:Ion Channels; D011942:Receptors, Adrenergic, alpha; D001030:Apamin; D000001:Calcimycin; D011803:Quinine; D011188:Potassium; D002118:Calcium; D009638:Norepinephrine