Urine concentrating defect in prostaglandin EP1-deficient mice.

Urine concentrating defect in prostaglandin EP1-deficient mice. Research Abstract Details 

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Urine concentrating defect in prostaglandin EP1-deficient mice. Abstract Text:

Chris R J Kennedy,Huaqi Xiong,Sherine Rahal,Jacqueline Vanderluit,Ruth S Slack,Yahua Zhang,Youfei Guan,Matthew D Breyer,Richard L ,

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.

Urine concentrating defect in prostaglandin EP1-deficient mice. Publishing Authors By Initials

CR Kennedy,H Xiong,S Rahal,J Vanderluit,RS Slack,Y Zhang,Y Guan,MD Breyer,RL ,

For similar behavior and behavior mechanisms: motivation: water deprivation research abstracts see: behavior and behavior mechanisms: motivation: water deprivation research

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Urine concentrating defect in prostaglandin EP1-deficient mice. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: American journal of physiology. Renal physiology

VOLUME: 292

Page Numbers: F868-75

Journal Abbreviation: Am. J. Physiol. Renal Physiol.

ISSN: 0363-6127

DAY: 1

MONTH: 08

YEAR: 2006

Urine concentrating defect in prostaglandin EP1-deficient mice. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901990

Urine concentrating defect in prostaglandin EP1-deficient mice. Keywords Mesh Terms:

KEYWORDS: Water Deprivation

MESH TERMS: physiology

Chemical & Substance for Abstract: Urine concentrating defect in prostaglandin EP1-deficient mice. Information

Substance Name: Deamino Arginine Vasopressin

Registry Number: 16679-58-6

Grant and Affiliation Information for Urine concentrating defect in prostaglandin EP1-deficient mice.

AFFILIATION: Department of Medicine, Ottawa Hospital, Ontario, Canada. ckennedy@uottawa.ca

Country: United States

AGENCY: United States NIDDK

GRANT: DK37097

ACRONYM: DK

MEDLINETA: Am J Physiol Renal Physiol

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