Mechanism of vasopressin-induced increase in intracellular Ca2+ in LLC-PK1 porcine kidney cells

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Abstract
Analysis of the signal transduction cascade of vasopressin-induced increase in intracellular Ca2+ concentration ([Ca2+]i) in LLC-PK1 cells was performed. First, a comparison of the effect of vasopressin on [Ca2+]i in LLC-PK1 cells with that produced in rat hepatocytes was performed [an intracellular mobilizing mechanism involving a V1 receptor coupled to the production of inositol 1,4,5-trisphosphate (IP3)]. Second, the effect of known inhibitors of intracellular Ca2+ mobilization on vasopressin Ca2+ response in LLC-PK1 cells was studied. Vasopressin induced a transient increase in [Ca2+]i in both LLC-PK1 cells and hepatocytes. In contrast to the single [Ca2+]i spike seen in LLC-PK1 cells, vasopressin induced an average of two to three [Ca2+]i spikes in hepatocytes. The V1 antagonist (Pmp1-O-Me-Tyr2-[Arg8]vasopressin, 1 microM) abolished vasopressin Ca2+ response in both cell types. Inhibitors of intracellular Ca2+ mobilization, thapsigargin (5 microM) and U-73122 (3 microM), abolished the Ca2+ response by vasopressin in LLC-PK1 cells. The results suggest that vasopressin-induced increase in [Ca2+]i in LLC-PK1 cells is mediated via a V1-like receptor and involves the mobilization of intracellular Ca2+ through an IP3- or thapsigargin-sensitive Ca2+ pool.

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