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

Kazuhisa Takeuchi, Nobuaki Yanai, Nobuyuki Takahashi, Takaaki Abe, Eikatsu Tsutsumi, Masuo Obinata, Keishi Abe

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16 Citations (Scopus)

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 V1 or V2 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 Ca2+ and prostaglandin (PG) E2 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 Ca2+ or inhibition of cyclooxygenase attenuated both VP-induced PGE2 synthesis and cAMP formation. In conclusion, both V1 and V2 receptors can stimulate cAMP formation. V1 receptor, however, stimulates cAMP formation via Ca2+-dependent PGE2 synthesis, whereas V2 receptor may stimulate it directly.

Original languageEnglish
Pages (from-to)680-687
Number of pages8
JournalBiochemical and biophysical research communications
Volume202
Issue number2
DOIs
Publication statusPublished - 1994 Jan 1

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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