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Pertussis toxin does not inhibit α 1 -adrenergic potentiation of β-adrenergic stimulation of cyclic AMP accumulation in rat pinealocytes

Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 168, Issue: 2, Page: 871-877
1990
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Article Description

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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