Renal cortical cyclooxygenase 2 expression is differentially regulated by angiotensin II AT(1) and AT(2) receptors.

Renal cortical cyclooxygenase 2 expression is differentially regulated by angiotensin II AT(1) and AT(2) receptors. Research Abstract Details 

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Renal cortical cyclooxygenase 2 expression is differentially regulated by angiotensin II AT(1) and AT(2) receptors. Abstract Text:

Ming-Zhi Zhang,Bing Yao,Hui-Fang Cheng,Su-Wan Wang,Tadashi Inagami,Raymond C Harris,

Macula densa cyclooxygenase 2 (COX-2)-derived prostaglandins serve as important modulators of the renin-angiotensin system, and cross-talk exists between these two systems. Cortical COX-2 induction by angiotensin-converting enzyme (ACE) inhibitors or AT(1) receptor blockers (ARBs) suggests that angiotensin II may inhibit cortical COX-2 by stimulating the AT(1) receptor pathway. In the present studies we determined that chronic infusion of either hypertensive or nonhypertensive concentrations of angiotensin II attenuated cortical COX-2. Angiotensin II infusion reversed cortical COX-2 elevation induced by ACE inhibitors. However, we found that angiotensin II infusion further stimulated cortical COX-2 elevation induced by ARBs, suggesting a potential role for an AT(2) receptor-mediated pathway when the AT(1) receptor was inhibited. Both WT and AT(2) receptor knockout mice were treated for 7 days with either ACE inhibitors or ARBs. Cortical COX-2 increased to similar levels in response to ACE inhibition in both knockout and WT mice. In WT mice ARBs increased cortical COX-2 more than ACE inhibitors, and this stimulation was attenuated by the AT(2) receptor antagonist PD123319. In the knockout mice ARBs led to significantly less cortical COX-2 elevation, which was not attenuated by PD123319. PCR confirmed AT(1a) and AT(2) receptor expression in the cultured macula densa cell line MMDD1. Angiotensin II inhibited MMDD1 COX-2, and CGP42112A, an AT(2) receptor agonist, stimulated MMDD1 COX-2. In summary, these results demonstrate that macula densa COX-2 expression is oppositely regulated by AT(1) and AT(2) receptors and suggest that AT(2) receptor-mediated cortical COX-2 elevation may mediate physiologic effects that modulate AT(1)-mediated responses.

Renal cortical cyclooxygenase 2 expression is differentially regulated by angiotensin II AT(1) and AT(2) receptors. Publishing Authors By Initials

MZ Zhang,B Yao,HF Cheng,SW Wang,T Inagami,RC Harris,

For similar proteins: carrier proteins: membrane transport proteins: ion pumps: symporters: sodium-potassium-chloride symporters research abstracts see: proteins: carrier proteins: membrane transport proteins: ion pumps: symporters: sodium-potassium-chloride symporters research

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Renal cortical cyclooxygenase 2 expression is differentially regulated by angiotensin II AT(1) and AT(2) receptors. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: Proceedings of the National Academy of Sciences of

VOLUME: 103

Page Numbers: 16045-50

Journal Abbreviation: Proc. Natl. Acad. Sci. U.S.A.

ISSN: 0027-8424

DAY: 16

MONTH: 10

YEAR: 2006

Renal cortical cyclooxygenase 2 expression is differentially regulated by angiotensin II AT(1) and AT(2) receptors. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7505876

Renal cortical cyclooxygenase 2 expression is differentially regulated by angiotensin II AT(1) and AT(2) receptors. Keywords Mesh Terms:

KEYWORDS: Sodium-Potassium-Chloride Symporters

MESH TERMS: metabolism

Chemical & Substance for Abstract: Renal cortical cyclooxygenase 2 expression is differentially regulated by angiotensin II AT(1) and AT(2) receptors. Information

Substance Name: Cyclooxygenase 2

Registry Number: EC 1.14.99.1

Grant and Affiliation Information for Renal cortical cyclooxygenase 2 expression is differentially regulated by angiotensin II AT(1) and AT(2) receptors.

AFFILIATION: George M. O'Brien Center for Research in Kidney and Urologic Diseases and Departments of Medicine and Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. ming-zhi.zhang@vanderbilt.edu

Country: United States

AGENCY: United States NIDDK

GRANT: P60 DK-20593

ACRONYM: DK

MEDLINETA: Proc Natl Acad Sci U S A

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