In:
American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 292, No. 5 ( 2007-05), p. F1418-F1426
Kurzfassung:
Vasopressin V 1a and V 2 receptors (V 1a R and V 2 R, respectively) distribute in the collecting duct of the kidney. Although the function of V 2 R mediating the antidiuretic effect of AVP has been investigated in detail, the role of V 1a R in the collecting ducts has not been elucidated. In the present study, we have investigated the role of the V 1a R pathway in V 2 R promoter activity. We cloned the 5′-flanking region of rat V 2 R (rV 2 R) and investigated rV 2 R promoter activity in the LLC-PK 1 cell line transfected to express rat V 1a R (rV 1a R) dominantly (LLC-PK 1 /rV 1a R). AVP induced a transient increase, followed by a sustained decrease, of rV 2 R promoter activity in these cells. This AVP-induced decrease of rV 2 R promoter activity was inhibited by V 1a R, but not V 2 R, antagonist. PMA mimicked this decrease of rV 2 R promoter activity. On the contrary, 8-(4-chlorophenylthio)-cAMP increased rV 2 R 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 V 2 R is downregulated via the V 1a R pathway in LLC-PK 1 /rV 1a R cells, and 2) expression of the V 2 R 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.
Materialart:
Online-Ressource
ISSN:
1931-857X
,
1522-1466
DOI:
10.1152/ajprenal.00358.2006
Sprache:
Englisch
Verlag:
American Physiological Society
Publikationsdatum:
2007
ZDB Id:
1477287-5
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