Mechanism of vasopressin-induced increase in intracellular Ca2+ in LLC-PK1 porcine kidney cells
Dibas, A.I.; Rezazadeh, S.M.; Vassan, R.; Mia, A.J.; Yorio, T.
American Journal of Physiology 272(3 Pt 1): C810-C817
1997
ISSN/ISBN: 0002-9513 PMID: 9124515 Document Number: 472468
Analysis of the signal transduction cascade of vasopressin-induced increase in intracellular Ca-2+ concentration ((Ca-2+)-i) in LLC-PK-1 cells was performed. First, a comparison of the effect of vasopressin on (Ca-2+)-i in LLC-PK-1 cells with that produced in rat hepatocytes was performed (an intracellular mobilizing mechanism involving a V-1 receptor coupled to the production of inositol 1,4,5-trisphosphate (IP-3)). Second, the effect of known inhibitors of intracellular Ca-2+ mobilization on vasopressin Ca-2+ response in LLC-PK-1 cells was studied. Vasopressin induced a transient increase in (Ca-2+)-i in both LLC-PK, cells and hepatocytes. In contrast to the single (Ca-2+)-i spike seen in LLC-PK-1 cells, vasopressin induced an average of two to three (Ca-2+)-i spikes in hepatocytes. The V-1 antagonist (Pmp-1-O-Me-Tyr-2(Arg-8)vasopressin, 1 mu-M) abolished vasopressin Ca-2+ response in both cell types. Inhibitors of intracellular Ca-2+ mobilization, thapsigargin (5 mu-M) and U-73122 (3 mu-M), abolished the Ca-2+ response by vasopressin in LLC-PK-1 cells. The results suggest that vasopressin-induced increase in (Ca-2+)-i in LLC-PK-1 cells is mediated via a V-1-like receptor and involves the mobilization of intracellular Ca-2+ through an IP-3- or thapsigargin-sensitive Ca-2+ pool.