Calcium-sensing Receptor Attenuates AVP-induced Aquaporin-2 Expression via a Calmodulin-dependent Mechanism | Zendy

Mauro Bustamante | Zendy; Udo Hasler | Zendy; ValeCombining Acute Accentrie Leroy | Zendy; Sophie de Seigneux | Zendy; Mitko Dimitrov | Zendy; David Mordasini | Zendy; Martine Rousselot | Zendy; PierreYves Martin | Zendy; Eric FeCombining Acute Accentraille | Zendy

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Calcium-sensing Receptor Attenuates AVP-induced Aquaporin-2 Expression via a Calmodulin-dependent Mechanism

Author(s) -

Mauro Bustamante,

Udo Hasler,

ValeCombining Acute Accentrie Leroy,

Sophie de Seigneux,

Mitko Dimitrov,

David Mordasini,

Martine Rousselot,

PierreYves Martin,

Eric FeCombining Acute Accentraille

Publication year - 2007

Publication title -

journal of the american society of nephrology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 4.451

H-Index - 279

eISSN - 1533-3450

pISSN - 1046-6673

DOI - 10.1681/asn.2007010092

Subject(s) - extracellular , medicine , calmodulin , endocrinology , vasopressin , aquaporin 2 , arginine vasopressin receptor 2 , calcium , calcium sensing receptor , chemistry , receptor , aquaporin 3 , biology , microbiology and biotechnology , aquaporin , calcium metabolism , antagonist , water channel , mechanical engineering , engineering , inlet

Recent evidence suggests that arginine vasopressin (AVP)-dependent aquaporin-2 expression is modulated by the extracellular calcium-sensing receptor (CaSR) in principal cells of the collecting duct, but the signaling pathways mediating this effect are unknown. Using a mouse cortical collecting duct cell line (mpkCCD(cl4)), we found that increasing the concentration of apical extracellular calcium or treating with the CaSR agonists neomycin or Gd(3+) attenuated AVP-dependent accumulation of aquaporin-2 mRNA and protein; CaSR gene-silencing prevented this effect. Calcium reduced the AVP-induced accumulation of cAMP, but this did not occur by increased degradation of cAMP by phosphodiesterases or by direct inhibition of adenylate cyclase. Notably, the effect of extracellular calcium on AVP-dependent aquaporin-2 expression was prevented by inhibition of calmodulin. In summary, our results show that high concentrations of extracellular calcium attenuate AVP-induced aquaporin-2 expression by activating the CaSR and reducing coupling efficiency between V(2) receptor and adenylate cyclase via a calmodulin-dependent mechanism in cultured cortical collecting duct cells.

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