Document Detail


Renal oxygenation defects in the spontaneously hypertensive rat: role of AT1 receptors.
MedLine Citation:
PMID:  12472784     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: The spontaneously hypertensive rat (SHR) has oxidative stress and enhanced O2 usage (Q(O2)) relative to tubular sodium transport (TNa). Angiotensin II (Ang II) acting on Type I receptors (AT1-R) causes renal oxidative stress and functional nitric oxide (NO) deficiency that could enhance O2 usage. Therefore, we investigated the hypothesis that AT1-Rs mediate the inefficient renal oxygenation in the SHR. METHODS: Groups of SHR and WKY received vehicle (Veh), candesartan (Cand) or hydralazine + hydrochlorothiazide + reserpine (HHR) for two weeks. RESULTS: Compared to WKY + Veh, the elevated BP of SHR + Veh (153 +/- 3 vs 115 +/- 3 mm Hg; P < 0.001) was normalized by Cand (117 +/- 4) or HHR (113 +/- 5 mm Hg). The reduced renal blood flow of SHR + Veh (2.4 +/- 0.3 vs. 4.1 +/- 0.3 mL. min-1. 100 g-1) was increased (P < 0.05) by Cand (3.6 +/- 0.3) and HHR (3.2 +/- 0.2). Compared to WKY + Veh, SHR + Veh had a 50% reduction in TNa: (16.9 +/- 2.0 vs. 7.8 +/- 0.9 micromol: micromol-1, P < 0.01) that was unchanged by HHR (8.6 +/- 1.1), but was increased by Cand (13.2 +/- 1.4; P < 0.01). The pO2 of outer cortex was lower in SHR + Veh than WKY + Veh (31 +/- 3 vs. 41 +/- 2 mm Hg; P < 0.05) and it was not changed significantly by HHR (37 +/- 2) but was normalized by Cand (44 +/- 3 mm Hg; P < 0.01). The pO2 in the deep cortex also was lower in SHR + Veh than WKY + Veh (18 +/- 3 vs. 30 +/- 3 mm Hg; P < 0.005) and was not changed significantly by HHR (19 +/- 2), but was increased by Cand (25 +/- 3 mm Hg; P < 0.05). CONCLUSIONS: The reduced pO2 in outer and inner cortex, and inefficient utilization of O2 for Na+ transport in the SHR kidney can be ascribed to the effects of AT1-R, largely independent of blood pressure.
Authors:
William J Welch; Horst Baumgärtl; Dietrich Lübbers; Christopher S Wilcox
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Kidney international     Volume:  63     ISSN:  0085-2538     ISO Abbreviation:  Kidney Int.     Publication Date:  2003 Jan 
Date Detail:
Created Date:  2002-12-10     Completed Date:  2004-03-02     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  United States    
Other Details:
Languages:  eng     Pagination:  202-8     Citation Subset:  IM    
Affiliation:
Division of Nephrology and Hypertension and Center for Hypertension and Renal Disease Research, Georgetown University, Washington, DC, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / metabolism
Blood Pressure
Body Weight
Hematocrit
Hypertension, Renal / metabolism*
Kidney Cortex / metabolism*
Male
Oxygen / metabolism*
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Receptor, Angiotensin, Type 1 / metabolism*
Sodium / metabolism
Grant Support
ID/Acronym/Agency:
DK-36079/DK/NIDDK NIH HHS; DK-49870/DK/NIDDK NIH HHS; HL6686-01/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Receptor, Angiotensin, Type 1; 7440-23-5/Sodium; 7782-44-7/Oxygen

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