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Am J Physiol Renal Physiol 292: F1274-F1282, 2007. First published December 26, 2006; doi:10.1152/ajprenal.00154.2006
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Downregulation of the V2 vasopressin receptor in dehydration: mechanisms and role of renal prostaglandin synthesis

¹Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, and ²Department of Pharmacy, Kumamoto University Hospital, Kumamoto, Japan

Submitted 2 May 2006 ; accepted in final form 22 December 2006

The vasopressin-aquaporin 2 system plays a key role in urine concentration in dehydration. In contrast to the upregulation of aquaporin 2, the downregulation of the vasopressin V2 receptor in dehydration is known. We investigated the mechanisms of this downregulation in dehydration using reverse transcription-competitive polymerase chain reaction (RT-competitive PCR) and Western blot analysis. The incubation of microdissected inner medullary collecting ducts (IMCDs) in a hypertonic medium or with vasopressin stimulated V2 receptor mRNA and protein expression, showing that dehydration-induced hyperosmolality in renal medulla and increased plasma arginine vasopressin (AVP) concentration should upregulate V2 receptor. The presence of inhibitory factors on the V2 receptor in dehydration was suggested. Prostaglandin E₂ (PGE₂) is known to inhibit AVP-induced cAMP production and to increase production in dehydration. PGE₂ slightly stimulated V2 receptor mRNA expression in IMCD in vitro. However, PGE₂ inhibited V2 receptor mRNA expression in IMCD in the presence of 10^–9 M vasopressin. The blockade of PGE₂ synthesis by indomethacin in dehydrated rats increased V2 receptor protein expression after 24–48 h with an early increase in V2 receptor mRNA expression. In summary, these data suggest that increased production of PGE₂ in renal medulla plays a key role in the downregulation of V2 receptor in dehydration.

V2 receptor; aquaporin 2; prostaglandin E₂; inner medullary collecting duct

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