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Downregulation of vasopressin V₂ receptor promoter activity via V_1a receptor pathway

Department of Nephrology, Graduate School of Medical Sciences, Kumamoto University, Kunamoto, Japan

Submitted 8 September 2006 ; accepted in final form 3 January 2007

Vasopressin V_1a and V₂ receptors (V_1aR and V₂R, respectively) distribute in the collecting duct of the kidney. Although the function of V₂R mediating the antidiuretic effect of AVP has been investigated in detail, the role of V_1aR in the collecting ducts has not been elucidated. In the present study, we have investigated the role of the V_1aR pathway in V₂R promoter activity. We cloned the 5'-flanking region of rat V₂R (rV₂R) and investigated rV₂R promoter activity in the LLC-PK₁ cell line transfected to express rat V_1aR (rV_1aR) dominantly (LLC-PK₁/rV_1aR). AVP induced a transient increase, followed by a sustained decrease, of rV₂R promoter activity in these cells. This AVP-induced decrease of rV₂R promoter activity was inhibited by V_1aR, but not V₂R, antagonist. PMA mimicked this decrease of rV₂R promoter activity. On the contrary, 8-(4-chlorophenylthio)-cAMP increased rV₂R promoter activity. These PMA- and 8-(4-chlorophenylthio)-cAMP-induced effects were not observed on the deletion segment of the 5'-flanking region lacking CAAT and SP1 sites. In conclusion, 1) expression of the V₂R is downregulated via the V_1aR pathway in LLC-PK₁/rV_1aR cells, and 2) expression of the V₂R is downregulated by the PMA-induced PKC pathway and upregulated by the cAMP-PKA pathway. These opposite effects of PKC and PKA appear to be regulated by the same promoter region of CAAT and SP1.

transcription regulation; collecting ducts

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