Phorbol esters inhibit alpha 1-adrenergic effects and decrease the affinity of liver cell alpha 1-adrenergic receptors for (-)-epinephrine.
作者： K R Schwarz , R M Graham , S Corvera , J A García-Sáinz
DOI: 10.1016/S0021-9258(17)36122-7
关键词:
摘要: 4 beta-Phorbol 12-myristate 13-acetate (PMA) modified the metabolic actions of three calcium-dependent hormones in different ways. The stimulations glycogenolysis ureogenesis and phosphatidylinositol labeling produced by alpha 1-adrenergic agonist was blocked phorbol ester. In contrast, PMA slightly increased stimulation low concentration angiotensin II without modifying maximal response. No effect observed on induced vasopressin. vasopressin decreased PMA, whereas that not affected. intact freshly isolated hepatocytes, [3H]prazosin binds with high affinity to a site which displays characteristics receptor. Competitive inhibition studies (-)-epinephrine reveal two sites for this agonist: (Kd 9 nM) 2 microM). presence esters, binding data now show single class sites, similar those present control cells. Thus, hepatocyte action may be related loss caused tumor promoter.
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