Role of alpha 1 adrenoceptors in the turnover of phosphatidylinositol and of alpha 2 adrenoceptors in the regulation of cyclic AMP accumulation in hamster adipocytes |
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Authors: | J A García-Sínz B B Hoffman S Y Li R J Lefkowitz J N Fain |
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Affiliation: | 1. Section of Physiological Chemistry, Division of Biology and Medicine, Brown University, Providence, Rhode Island 02912, USA;2. The Howard Hughes Medical Institute Laboratory, Department of Medicine and Biochemistry, Duke University Medical Center, Durham, North Carolina 27710, USA |
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Abstract: | The incorporation of radioactive phosphate into phosphatidylinositol was stimulated by epinephrine in hamster fat cells. This action was inhibited by alpha-adrenergic antagonists in the potency order: Prazosin?phentolamine>yohimbine. Methoxamine, but not clonidine, was able to mimic the effect of epinephrine. These data indicate that the phosphatidylinositol effect in fat cells is due to activation of alpha1 adrenoceptors. On the other hand, the accumulation of cyclic AMP due to epinephrine was potentiated by alpha-adrenergic antagonists in the potency order phentolamine>yohimbine ?prazosin, in hamster fat cells. Clonidine significantly decreased the accumulation of cyclic AMP due to isoproterenol or ACTH in hamster fat cells, suggesting that the alpha-adrenergic modulation of cyclic AMP levels in hamster fat cells is mediated by alpha2 adrenoceptors. Radioligand binding studies with plasma membranes from hamster adipocytes demonstrated the presence of both alpha1 and alpha2 adrenoceptors but about 90% of the binding sites were alpha2. These data support the hypothesis that alpha2 effects of catecholamines are due to inhibition of adenylate cyclase while the increases in phosphatidylinositol turnover that seem to be involved in the mobilization of calcium are linked exclusively to alpha1 adrenoceptor activation. |
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