Manipulation of Intracellular Calcium in NCB‐20 Cells

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Abstract
A number of lines of evidence indicate that the Ca2+ and cyclic AMP signalling systems interact in NCB‐20 cells. However, to date, the regulation of [Ca2+]i homeosta‐sis has not been studied in this cell line. The present study aimed to clarify our understanding of [Ca2+]i homeostasis in these cells and to evaluate tools that manipulate [Ca2+]i, independently of protein kinase C effects. Bradykinin, by a B2‐receptor, elevated [Ca2+]i by a pertussis‐toxin‐insensitive mechanism. The BK‐stimulated [Ca2+]i rise originated from intracellular sources, without a contribution from Ca2+ entry mechanisms. The effect of BK was precluded by pre‐treatment with thapsigargin and ionomycin—compounds that elevated [Ca2+]i independent of phospholipase C activation. Both compounds, however, exerted effects in addition to stimulating release of Ca2+ from BK‐sensitive stores; the BK‐sensitive Ca2+ pool was a subset of the thapsigargin‐sensitive pool; ionomycin strongly stimulates Ca2+ entry. Activation of protein kinases A and C attenuated the duration of the BK‐induced rise in [Ca2+]i, without affecting the peak [Ca2+]i, suggesting interference with the BK response at a step downstream of the activation of phospholipase C. Application of these approaches should enhance the delineation of the consequences of Ca2+ mobilization on cyclic AMP accumulation.

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