In PC Cl3 rat thyroid cell line noradrenaline-induced Ca2+ response, mainly due to the activation of α1B receptors, is characterized by a rapid peak phase, due to the Ca2+ mobilization from inositol trisphosphate-sensitive internal stores, followed by a sustained plateau, representing the capacitative calcium entry. The plateau phase elicited by noradrenaline returns to the basal value within 100 sec from the removal of agonist. The tyrosine kinases inhibitor genistein completely abolishes the plateau upon noradrenaline withdrawl. On the contrary, the tyrosine phosphatases blocker, vanadate, potentiates the plateau phase of calcium response to noradrenaline and prevents the gradual decrease of [Ca2+]i after removal of noradrenaline. The noradrenaline-induced Ca2+ influx, due to the activation of α1A receptor-operated Ca2+ entry is not affected by vanadate. The treatment with noradrenaline induced the tyrosine phosphorylation of specific substrates in lysates derived from PC Cl3 cells, an effect inhibited by genistein pretreatment. These results show that a balance between tyrosine phosphorylation and dephosphorylation is required for the regulation of capacitative calcium entry following noradrenaline stimulation of α1B receptor, whilst the influx of Ca2+ directly operated by α1A receptor activation seems to be independent of the tyrosine phosphorylating pathway.
|Number of pages||9|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Apr 17 1995|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology