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Abstract

Evidence suggests that GTP but not GTP_γS activates Ca²⁺ movement between myo-inositol 1,4,5-trisphoshate (IP₃)-sensitive and -insensitive Ca²⁺ pools (1). Measuring ⁴⁵Ca²⁺ uptake into pancreatic microsomal vesicles we have determined the sizes of three different Ca²⁺ pools which release Ca²⁺ in response 1) to IP₃, 2) to caffeine, and 3) to both IP₃ and caffeine (“common” Ca²⁺ pool). In the presence of GTP the size of the IP₃-sensitive Ca²⁺ pool is decreased whereas the “common” Ca²⁺ pool is increased as compared to control Ca²⁺ pool sizes in the presence of GTP_γS. This effect of GTP is inhibited by bafilomycin B₁, a specific inhibitor of vacuolar type H⁺ ATPases (2). We conclude that GTP induced connection between IP₃ and caffeine-sensitive Ca²⁺ pools is triggered by intravesicular acidification and involves function of small GTP-binding proteins, known to mediate interorganelle transfer.