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Am J Physiol Cell Physiol 253: C301-C308, 1987;
0363-6143/87 $5.00
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AJP - Cell Physiology, Vol 253, Issue 2 C301-C308, Copyright © 1987 by American Physiological Society

ARTICLES

Distinction between mechanisms underlying alpha 1- and beta-adrenergic respiratory stimulation in brown fat cells

N. Mohell, E. Connolly and J. Nedergaard

Experimental conditions are described for selective alpha 1- and beta-adrenergic stimulation of the respiration of brown fat cells. The dual agonist norepinephrine was unsuitable as a selective alpha 1-agonist, since unacceptably high concentrations of propranolol were needed to abolish the beta-response. Phenylephrine at 50 microM, in the presence of 5 microM dl-propranolol, was shown to lead to a maximal, selective alpha 1-stimulation, whereas maximal, selective beta-stimulation was achieved with 1 microM isoproterenol in the presence of 5 microM prazosin. The mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) was able to further increase respiration that was already maximally alpha 1-stimulated, but when added before the alpha 1-stimulation, FCCP totally abolished the response. In contrast, FCCP had no effect on the beta-stimulated response. Similarly, oligomycin (an inhibitor of mitochondrial ATP synthesis) inhibited alpha 1-respiration but had a much smaller effect on beta-respiration. Ouabain (an inhibitor of the Na+-K+-ATPase) halved alpha 1-respiration but only induced a small inhibition of beta-respiration. It is concluded that only a small fraction of thermogenesis from beta-adrenergic processes is due to oxidative phosphorylation, whereas alpha 1-respiration is largely due to the oxygen cost of mitochondrial ATP synthesis, and a large fraction of this ATP is apparently used for the restoration of ion gradients.


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