TY - JOUR
T1 - 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
AU - Takeuchi, Kazuhisa
AU - Yanai, Nobuaki
AU - Takahashi, Nobuyuki
AU - Abe, Takaaki
AU - Tsutsumi, Eikatsu
AU - Obinata, Masuo
AU - Abe, Keishi
PY - 1994/1/1
Y1 - 1994/1/1
N2 - 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.
AB - 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.
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U2 - 10.1006/bbrc.1994.1984
DO - 10.1006/bbrc.1994.1984
M3 - Article
C2 - 8048937
AN - SCOPUS:0028067490
VL - 202
SP - 680
EP - 687
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 2
ER -