Abstract
Cell swelling-induced insulin secretion represents an alternative pathway of stimulation of insulin secretion. INS-1E rat tumor beta cells do not release insulin in response to cell swelling in presence of Ca<sup>2+</sup> despite a good response to glucose challenge and appropriate increase in cell volume. Surprisingly, perifusion with Ca<sup>2+</sup>-depleted medium showed distinct secretory response of INS-1E cells to hypotonicity. Objective of this study was further characterization of the role of Ca<sup>2+</sup> in secretory process in INS-1 and INS-1E cell lines. Ca<sup>2+</sup> depleted hypotonic medium with 10 µM BAPTA/AM (intracellular chelator) induced insulin secretion from both types of cells. We demonstrated expression of L-type Ca<sup>2+</sup> channel Ca<sub>v</sub>1.2 and non-L-type Ca<sup>2+</sup> channels Ca<sub>v</sub>2.1 (P/Q-type), Ca<sub>v</sub>2.2 (N-type), and Ca<sub>v</sub>3.1 (T-type) in both cell lines. Inhibition of L type channel with nifedipine and/or P/Q type with ω-agatoxin IVA enabled distinct response to hypotonic medium also in INS-1E cells. Tetanus toxin (TeTx) in medium containing Ca<sup>2+</sup> and a group of calcium channel blockers inhibited hypotonicity-induced insulin secretion from INS-1 cells but not from INS-1E cells. Conclusion: Hypotonicity-induced insulin secretion from INS-1E cells is inhibited by extracellular Ca<sup>2+</sup>, does not require intracellular Ca<sup>2+</sup> and is TeTx resistant.
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