Noradrenaline stimulates not only Ca2+ mobilization but also cAMP formation through activation of α1-adrenoceptors in hepatocytes from mature male rats. We examined which subtype(s) of α1-adrenoceptor mediate these signal transduction mechanisms. Treatment of hepatocytes with chloroethylclonidine produced a dose-dependent inhibition of noradrenaline-induced Ca2+ mobilization, involving both transient and sustained components. Chloroethylclonidine also blocked noradrenaline-induced cAMP accumulation. It was observed that prazosin was much more potent than WB4101 (2-(2,6-dimethoxy-phenoxyethyl)aminomethyl-1,4-benzodioxane) in antagonizing noradrenaline-induced Ca2+ mobilization. The same potency order was found in cAMP formation studies. Pretreatment of rats with pertussis toxin did not affect α1-adrenergic responsiveness. Incubations of hepatocytes with tumor-promoting phorbol esters eliminated both Ca2+ mobilization and cAMP accumulation caused by noradrenaline. Our data suggest that in hepatocytes from mature male rats, single α1B-adrenoceptors are linked to cAMP formation as well as Ca2+ mobilization.
|Number of pages||8|
|Journal||European Journal of Pharmacology: Molecular Pharmacology|
|Publication status||Published - 15-07-1993|
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