Discrepancy in the regulatory effects of sodium and guanine nucleotides on adrenaline and clonidine binding to alpha 2-adrenoceptors in human fat cell membranes.
Guanine nucleotides and sodium were found to reduce the affinity of adrenaline for the alpha 2-adrenoceptor sites labelled by [3H]yohimbine in human fat cell membranes. Surprisingly, the negative regulation by these agents was far weaker when clonidine, the alpha 2-agonist prototype was used. The results are discussed in relation to the weaker or the lack of adenylate cyclase inhibition promoted by clonidine and indicate that the formation of the lower affinity state of the alpha-receptor is essential to the alpha 2-adrenoceptor-mediated adenylate cyclase inhibition.
D000273:Adipose Tissue / Q000378:metabolism*; D001665:Binding Sites; D002462:Cell Membrane / Q000378:metabolism; D003000:Clonidine / Q000378:metabolism*; D004837:Epinephrine / Q000378:metabolism*; D006150:Guanine Nucleotides / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D011941:Receptors, Adrenergic / Q000378:metabolism*; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D012964:Sodium / Q000494:pharmacology*; D015016:Yohimbine / Q000378:metabolism
D006150:Guanine Nucleotides; D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D015016:Yohimbine; D012964:Sodium; D003000:Clonidine; D004837:Epinephrine