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1 Department of Nephrology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Kumamoto, Japan
2 Kumamoto, Kumamoto, Japan; Department of Nephrology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Kumamoto, Japan
3 Department of Nephrology, Graduate School of Medical Sciences, Kumamoto University, kumamoto, Kumamoto, Japan
4 kumamoto, Kumamoto, Japan; Department of Nephrology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Kumamoto, Japan
* To whom correspondence should be addressed. E-mail: 053r5110{at}med.stud.kumamoto-u.ac.jp.
Vasopressin V1a and V2 receptors (V1aR and V2R, respectively) distribute in the collecting duct of the kidney. While the function of V2R mediating antidiuretic effect of AVP has been investigated in detail, the role of V1aR in the collecting ducts has not been elucidated. In the present study, we investigated the role of V1aR pathway in V2R promoter activity. We cloned 5' flanking region of rat V2R (rV2R) and investigated rV2R promoter activity in LLC-PK1 cell line transfected to express rat V1aR (rV1aR) dominantly (LLC-PK1/rV1aR). After transient increase, sustained decrease of rV2R promoter activity was observed by the treatment with AVP in these cells. This decrease of rV2R promoter activity by AVP was inhibited by V1aR antagonist but not by V2R antagonist. PMA mimicked this decrease of rV2R promoter activity. On the contrary, cpt-cAMP increased rV2R promoter activity. These effects caused by PMA and cpt-cAMP were not observed on the deletion segment of 5' flanking region lacking CAAT and SP1 sites. In conclusion, 1) The expression of V2R is down-regulated via V1aR pathway in LLC-PK1/rV1aR cells. 2) The expression of V2R is down-regulated by PMA-induced PKC pathway and up-regulated by cAMP-PKA pathway. These opposite effects of PKC and PKA appear to be regulated by the same promoter region of CAAT and SP1.
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