In:
American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 292, No. 2 ( 2007-02), p. F868-F875
Abstract:
We investigated the role of the prostaglandin E 2 (PGE 2 ) EP 1 receptor in modulating urine concentration as it is expressed along the renal collecting duct where arginine-vasopressin (AVP) exerts its anti-diuretic activity, and in the paraventricular and supraoptic nuclei of the hypothalamus where AVP is synthesized. The urine osmolality of EP 1 -null mice (EP 1 −/− ) failed to match levels achieved by wild-type (WT) counterparts upon water deprivation (WD) for 24 h. This difference was reflected by higher plasma osmolality in WD EP 1 −/− mice. Along the collecting duct, the induction and subapical to plasma membrane translocation of the aquaporin-2 water channel in WD EP 1 −/− mice appeared equivalent to that of WD WT mice as determined by quantitative RT-PCR and immunohistochemistry. However, medullary interstitial osmolalities dropped significantly in EP 1 −/− mice following WD. Furthermore, urinary AVP levels of WD EP 1 −/− mice were significantly lower than those of WD WT mice. This deficit could be traced back to a blunted induction of hypothalamic AVP mRNA expression in WD EP 1 −/− mice as determined by quantitative RT-PCR. Administration of the AVP mimetic [deamino-Cys 1 ,d-Arg 8 ]-vasopressin restored a significant proportion of the urine concentrating ability of WD EP 1 −/− mice. When mice were water loaded to suppress endogenous AVP production, urine osmolalities increased equally for WT and EP 1 −/− mice. These data suggest that PGE 2 modulates urine concentration by acting at EP 1 receptors, not in the collecting duct, but within the hypothalamus to promote AVP synthesis in response to acute WD.
Type of Medium:
Online Resource
ISSN:
1931-857X
,
1522-1466
DOI:
10.1152/ajprenal.00183.2005
Language:
English
Publisher:
American Physiological Society
Publication Date:
2007
detail.hit.zdb_id:
1477287-5
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