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Electrochemical detection of quantal catecholamine release from PC-12 cells revealed that glibenclamide, an inhibitor of ATP-sensitive K+ channels, potentiated Ca2+-dependent exocytosis evoked by raised extracellular [K+] and by exposure of cells to caffeine. Glibenclamide was without effect on voltage-gated Ca2+ currents, membrane potential, or rises of [Ca2+]i evoked by either raised extracellular [K+] or caffeine. The dependence of K+-evoked secretion on extracellular Ca2+ was shifted leftward in the presence of glibenclamide, with a small increase in the plateau level of release, suggesting that glibenclamide primarily increased the Ca2+ sensitivity of the exocytotic apparatus. Enhancement of secretion by glibenclamide was reversed by pinacidil and cromakalim, indicating that the effects of glibenclamide were mediated via an action on a sulfonylurea receptor. These results demonstrate that sulfonylurea receptors can modulate Ca2+-dependent exocytosis via a mechanism downstream of Ca2+ influx or mobilization.

the journal of neuroscience/the journal of neuroscience

Potentiation of Quantal Catecholamine Secretion by Glibenclamide: Evidence for a Novel Role of Sulphonylurea Receptors in Regulating the Ca<sup>2+</sup>Sensitivity of Exocytosis

Potentiation of Quantal Catecholamine Secretion by Glibenclamide: Evidence for a Novel Role of Sulphonylurea Receptors in Regulating the Ca2+Sensitivity of Exocytosis

Potentiation of Quantal Catecholamine Secretion by Glibenclamide: Evidence for a Novel Role of Sulphonylurea Receptors in Regulating the Ca²⁺Sensitivity of Exocytosis