Alpha 1-adrenergic stimulation of hamster brown adipocyte respiration

Publisher Website
Google Scholar
Abstract
Respiration was increased approximately 5-fold with 0.05 microM norepinephrine and to a maximum of 10-fold by 0.30 microM norepinephrine. Prazosin, an alpha-adrenergic blocking agent highly selective for alpha 1-type receptors, partially inhibited the response to norepinephrine (0.05 microM) by 20-25% at a concentration of 0.10-1 microM. In contrast, when the stimulus for respiration was provided by isoproterenol or 3-isobutyl-1-methylxanthine, prazosin was without effect up to a concentration of 10 microM. Yohimbine, an alpha-adrenergic blocking drug preferential for alpha 2-receptors, did not influence norepinephrine-stimulated oxygen uptake. Respiration was increased two- to fourfold by phenylephrine or methoxamine, agents preferential for alpha 1-adrenergic receptors but not at all by clonidine, an agent preferential for alpha 2-adrenergic receptors. The stimulatory effect of phenylephrine on oxygen uptake was fully blocked by prazosin but not propranolol. Removal of extracellular calcium with ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid prevented phenylephrine stimulation of respiration but was without effect when isoproterenol was the stimulus. These results support the participation of alpha 1-adrenergic receptors in control of respiration and are consistent with the possibility that changes in cell calcium are intimately involved in this response.