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  • Title: Inhibitory action of guanfacine on glucose uptake by adipose tissue not related to its alpha 2-adrenergic stimulatory potency.
    Author: Von Bruchhausen F.
    Journal: Arzneimittelforschung; 1985; 35(12):1813-5. PubMed ID: 2869761.
    Abstract:
    Because of its N-amidino-carboxamide structure, the action of guanfacine on the formation of 14CO2 from [1-14C]-glucose and on the decrease in glucose in the external medium was studied in rat adipose tissue. Both the formation of 14CO2 and the decrease in glucose in the external medium are inhibited by guanfacine in the absence as well as in the presence of insulin. A half maximum effect occurs at 10-4 mol/l. The inhibitory effect is of a competitive nature and is equally evident in isolated fat cells. The transport of [14C]-desoxyglucose into adipocytes in the presence of guanfacine is also lower than it is normally. Clonidine at equal concentrations does not show such an inhibitory effect. Antagonistically effective concentrations of the alpha 2-antagonist yohimbine do not abolish the effect of guanfacine. For this reason, because of the doubts concerning the existence of alpha 2-receptors in rat adipose tissue, and because of the fact that higher concentrations are needed, the observed inhibitory effect on the uptake of glucose into the adipose tissue is not considered as a consequence of an alpha 2-stimulation. As the inhibitory effect is maintained with an external medium with a low content of Na+, it cannot be explained by a restriction of the Na+/H+ antiport.
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