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Different Cellular Mechanisms of Vasopressin Receptor V1 and V2 Subtype in Vasopression-Induced Adenosine 3′,5′-Monophosphate Formation in an Immortalized Renal Tubule Cell Line, TKC2

Authors
Journal
Biochemical and Biophysical Research Communications
0006-291X
Publisher
Elsevier
Publication Date
Volume
202
Issue
2
Identifiers
DOI: 10.1006/bbrc.1994.1984

Abstract

Abstract Vasopressin (VP) stimulates adenosine 3′,5′-monophosphate (cAMP) formation in an immortalized renal tubule cell line, TKC2, which is derived from transgenic mouse harboring temperature-sensitive SV40 T-antigen gene. VP (10 −8 M)induced cAMP formation was significantly attenuated by either non-peptide vasopressin receptor V 1 or V 2 subtype antagonist, OPC-21268 (10 −8 and 10 −6 M) or OPC-31260 (10 −8 and 10 −6 M), respectively, and it was completely abolished by combination of both agents (10 −6 M). VP (10 −8 M) also induced an increase in cytosolic free Ca 2+ and prostaglandin (PG) E 2 synthesis, both of which were significantly inhibited by OPC-21268 (10 −8 M), but not by OPC-31260 (10 −6 M). Either OPC-21268 (10 −8 M), depletion of extracellular Ca 2+ or inhibition of cyclooxygenase attenuated both VP-induced PGE 2 synthesis and cAMP formation. In conclusion, both V 1 and V 2 receptors can stimulate cAMP formation. V 1 receptor, however, stimulates cAMP formation via Ca 2+-dependent PGE 2 synthesis, whereas V 2 receptor may stimulate it directly.

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