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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 1969 Sep;64(1):113–120. doi: 10.1073/pnas.64.1.113

NOREPINEPHRINE-INDUCED DEPOLARIZATION OF BROWN FAT CELLS*

B A Horwitz 1,2, J M Horowitz Jr 1,2, R Em Smith 1,2
PMCID: PMC286134  PMID: 5262992

Abstract

Intracellular potentials of brown fat cells in lightly anesthetized cold-acclimated rats were measured in vivo. The effects of adrenergic agonists and antagonists on these potentials were examined in an attempt to relate the electrical activity of the cells to the adrenergic-induced stimulation of brown fat thermogenesis.

Norepinephrine, the physiological mediator of brown fat heat production, significantly depolarized the membrane of these cells in vivo. This was effected either upon norepinephrine administration (3-100 μg/kg body wt) or excitation of the transsected nerve trunk to the interscapular fat pad and appreciably inhibited (55%) by doses of propranolol (1 mg/kg) sufficient to abolish the temperature increase of the tissue. Since theophylline (325 μm/kg) did not depolarize the cells, although it stimulated thermogenesis in the tissue, the depolarizing effect of norepinephrine is interpreted as being at least partially associated with biochemical events terminating in the activation of adenylate cyclase. However, the norepinephrine-induced electrical changes and the ensuing increase in brown fat thermogenesis appear to be causally independent and experimentally separable. On the other hand, our data do not preclude the speculation that the membrane phenomenon, if accompanied by increased Na+, may serve partially to regulate the metabolic rate of brown fat during long-term physiological stimulation (e.g., cold stress) by increasing the rate of ATP utilization via the Na+/K+ pump.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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