Abstract
The hypothesis that G i might be involved in the α 1-adrenergic, protein kinase C (PKC)-mediated amplification of β-adrenergic cyclic AMP stimulation in rat pinealocytes was investigated. Treatment of pinealocytes with a high concentration of pertussis toxin (500 ng/ml, 18 h) almost completely (approximately 95%) inactivated two cell membrane G-proteins (kDa 40.7 and 39.8) judged by back ADP-ribosylation of pinealocyte membrane proteins. However, this treatment failed to inhibit either the β-adrenergic (isoprepaline, ISO 10 −6 M), α 1-plus β-adrenergic (noradrenaline, NA 10 −5 M) or β -adrenergic plus 12-O-tetradecanoylphorbol 13-acetate (TPA 10 −7 M) induced stimulation of cyclic AMP or cyclic GMP. These results suggest that α 1-adrenergic potentiation of β-adrenergic stimulation of cyclic AMP and cyclic GMP does not involve a pertussis toxin-sensitive G-protein.
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