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Volume 272, Number 52, Issue of December 26, 1997 pp. 32847-32856

₁-Adrenergic Stimulation Potentiates the Thermogenic Action of ₃-Adrenoreceptor-generated cAMP in Brown Fat Cells

(Received for publication, July 18, 1997, and in revised form, September 10, 1997)

From the Wenner-Gren Institute, the Arrhenius Laboratories F3, Stockholm University, S-106 91 Stockholm, Sweden

The relationship between cAMP levels and thermogenesis was investigated in brown fat cells from Syrian hamsters. Irrespective of whether the selective ₃-, ₂-, and ₁-agonists BRL 37344, salbutamol, and dobutamine or the physiological agonist norepinephrine was used to stimulate the cells, increases in cAMP levels were mediated via the ₃-receptor, as were the thermogenic effects. However, the relationship "thermogenesis per cAMP" was much lower for agents other than norepinephrine. Similarly, forskolin, although more potent than norepinephrine in elevating cAMP, was less potent in inducing thermogenesis. The selective ₁-agonist cirazoline was in itself without effect on cAMP levels or thermogenesis, but when added to forskolin-stimulated cells, potentiated thermogenesis, up to the norepinephrine level, without affecting cAMP. This potentiation could not be inhibited by chelerythrine, but could be mimicked by Ca²⁺ ionophores. It was apparently not mediated via calmodulin-dependent protein kinase and was not an effect on mitochondrial respiratory control. The ability of all cAMP-elevating agents to induce thermogenesis in brown fat cells has earlier been interpreted to mean that it is only through the -receptors and the resulting increase in cAMP levels that thermogenesis is induced. However, it is here concluded that the thermogenic response to norepinephrine involves two interacting parts, one mediated via -receptors and cAMP and the other via ₁-receptors and increases in cytosolic Ca²⁺ levels.

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