Nicotine-like effects of cotinine on protein kinase C activity and noradrenaline release in bovine adrenal chromaffin cells
Article first published online: 9 OCT 2008
Journal of Autonomic Pharmacology
Volume 18, Issue 4, pages 245–250, August 1998
How to Cite
Vainio, P. J., Viluksela, M. and Tuominen, R. K. (1998), Nicotine-like effects of cotinine on protein kinase C activity and noradrenaline release in bovine adrenal chromaffin cells. Journal of Autonomic Pharmacology, 18: 245–250. doi: 10.1046/j.1365-2680.1998.18490.x
- Issue published online: 9 OCT 2008
- Article first published online: 9 OCT 2008
- Cited By
1 We studied the effect of cotinine, a slowly eliminated metabolite of nicotine, on protein kinase C (PKC) distribution and noradrenaline release in primary cultured bovine adrenal chromaffin cells. Changes in PKC activity were detected by [3H]-phorbol-12,13-dibutyrate binding, histone phosphorylation assay and by Western blot.
2 Cotinine (10–32 mm) increased phorbol binding to chromaffin cells in response to 10 min but not to 24 h exposure. The increased binding was reversed by a nicotinic antagonist hexamethonium (10 μm).
3 Cotinine (10 mm, 30 min) also increased membrane-associated PKC activity and membrane-associated PKC α and ε immunoreactivity.
4 Cotinine (0.1–32 mm for 10 s to 20 min) dose- and time-dependently increased the release of preloaded [3H]-noradrenaline from the cultured cells. The release increased with increasing duration of the contact period. In treatments lasting 1 min or longer, a peak effect was followed by a reduced response at higher concentrations.
5 We confirm the earlier findings that cotinine is biologically active, and conclude that its effects are at least partly mediated via nicotinic cholinergic receptors and through PKC.