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Presence of a Ca2+-dependent K+ channel in brown adipocytes. Possible role in maintenance of alpha 1-adrenergic stimulation.
The Wenner-Gren Institute, University of Stockholm.
1985 (English)In: Biochimica et Biophysica Acta, ISSN 0006-3002, Vol. 844, no 1, 42-49 p.Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
1985. Vol. 844, no 1, 42-49 p.
National Category
Medical and Health Sciences
Research subject
Biomedical Sciences
URN: urn:nbn:se:kau:diva-29825PubMedID: 2578297OAI: diva2:657589
Available from: 2013-10-21 Created: 2013-10-21 Last updated: 2013-10-28Bibliographically approved

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