Vasopressin stimulates Na-dependent phosphate transport and calcification in rat aortic smooth muscle cells

Keiko Nishiwaki-Yasuda, Atsushi Suzuki, Ayako Kakita, Sahoko Sekiguchi, Shogo Asano, Kazuhiro Nishii, Shizuko Nagao, Yutaka Oiso, Mitsuyasu Itoh

Research output: Contribution to journalArticle

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Abstract

We investigated the effect of arginine vasopressin (AVP) on inorganic phosphate (Pi) transport in A-10 rat aortic vascular smooth muscle cells (VSMCs). AVP time- and dose-dependently stimulated Na-dependent Pi transport in A-10 cells. This stimulatory effect of AVP on Pi transport was markedly suppressed by V1 receptor antagonist. A protein kinase C (PKC) inhibitor calphostin C partially suppressed the stimulatory effect of AVP. The selective inhibitors of c-Jun-NH2-terminal mitogen-activated protein (MAP) kinase (Jun kinase) attenuated AVP-induced Pi transport, but Erk kinase or p38 MAP kinase inhibitors did not. Wortmannin, a phosphatidylinositol (PI) 3-kinase inhibitor, suppressed AVP-induced Pi transport. Rapamycin, a selective inhibitor of S6 kinase, reduced this effect of AVP, while Akt kinase inhibitor did not. The combination of inhibitors for PKC, Jun kinase and PI 3-kinase completely suppressed the AVP-enhanced Pi transport. Furthermore, AVP rescued the VSMC from high phosphate-induced cell death and enhanced mineralization of these cells. In summary, these results suggest that AVP stimulates both Na-dependent Pi transport and mineralization in VSMCs. The mechanism is mediated by the activation of multiple signaling pathways including PKC, PI 3-kinase, S6 kinase and Jun kinase.

Original languageEnglish
Pages (from-to)103-112
Number of pages10
JournalEndocrine Journal
Volume54
Issue number1
DOIs
Publication statusPublished - 30-03-2007

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Arginine Vasopressin
Vasopressins
Smooth Muscle Myocytes
Phosphates
Phosphatidylinositol 3-Kinase
Vascular Smooth Muscle
Ribosomal Protein S6 Kinases
Phosphotransferases
antineoplaston A10
Protein Kinase Inhibitors
Protein Kinase C
Vasopressin Receptors
Protein C Inhibitor
Mitogen-Activated Protein Kinase Kinases
p38 Mitogen-Activated Protein Kinases
Sirolimus
Cell Death

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Nishiwaki-Yasuda, Keiko ; Suzuki, Atsushi ; Kakita, Ayako ; Sekiguchi, Sahoko ; Asano, Shogo ; Nishii, Kazuhiro ; Nagao, Shizuko ; Oiso, Yutaka ; Itoh, Mitsuyasu. / Vasopressin stimulates Na-dependent phosphate transport and calcification in rat aortic smooth muscle cells. In: Endocrine Journal. 2007 ; Vol. 54, No. 1. pp. 103-112.
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Nishiwaki-Yasuda, K, Suzuki, A, Kakita, A, Sekiguchi, S, Asano, S, Nishii, K, Nagao, S, Oiso, Y & Itoh, M 2007, 'Vasopressin stimulates Na-dependent phosphate transport and calcification in rat aortic smooth muscle cells', Endocrine Journal, vol. 54, no. 1, pp. 103-112. https://doi.org/10.1507/endocrj.K06-093

Vasopressin stimulates Na-dependent phosphate transport and calcification in rat aortic smooth muscle cells. / Nishiwaki-Yasuda, Keiko; Suzuki, Atsushi; Kakita, Ayako; Sekiguchi, Sahoko; Asano, Shogo; Nishii, Kazuhiro; Nagao, Shizuko; Oiso, Yutaka; Itoh, Mitsuyasu.

In: Endocrine Journal, Vol. 54, No. 1, 30.03.2007, p. 103-112.

Research output: Contribution to journalArticle

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T1 - Vasopressin stimulates Na-dependent phosphate transport and calcification in rat aortic smooth muscle cells

AU - Nishiwaki-Yasuda, Keiko

AU - Suzuki, Atsushi

AU - Kakita, Ayako

AU - Sekiguchi, Sahoko

AU - Asano, Shogo

AU - Nishii, Kazuhiro

AU - Nagao, Shizuko

AU - Oiso, Yutaka

AU - Itoh, Mitsuyasu

PY - 2007/3/30

Y1 - 2007/3/30

N2 - We investigated the effect of arginine vasopressin (AVP) on inorganic phosphate (Pi) transport in A-10 rat aortic vascular smooth muscle cells (VSMCs). AVP time- and dose-dependently stimulated Na-dependent Pi transport in A-10 cells. This stimulatory effect of AVP on Pi transport was markedly suppressed by V1 receptor antagonist. A protein kinase C (PKC) inhibitor calphostin C partially suppressed the stimulatory effect of AVP. The selective inhibitors of c-Jun-NH2-terminal mitogen-activated protein (MAP) kinase (Jun kinase) attenuated AVP-induced Pi transport, but Erk kinase or p38 MAP kinase inhibitors did not. Wortmannin, a phosphatidylinositol (PI) 3-kinase inhibitor, suppressed AVP-induced Pi transport. Rapamycin, a selective inhibitor of S6 kinase, reduced this effect of AVP, while Akt kinase inhibitor did not. The combination of inhibitors for PKC, Jun kinase and PI 3-kinase completely suppressed the AVP-enhanced Pi transport. Furthermore, AVP rescued the VSMC from high phosphate-induced cell death and enhanced mineralization of these cells. In summary, these results suggest that AVP stimulates both Na-dependent Pi transport and mineralization in VSMCs. The mechanism is mediated by the activation of multiple signaling pathways including PKC, PI 3-kinase, S6 kinase and Jun kinase.

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