Document Detail


TNFR1-deficient mice display altered blood pressure and renal responses to ANG II infusion.
MedLine Citation:
PMID:  20739394     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The hypothesis that TNF receptor 1-deficient (TNFR1(-/-)) mice display blood pressure (BP) and renal functional responses that differ from wild-type (WT) mice was tested in an angiotensin II (ANG II)-dependent model of hypertension. Basal systolic BP (SBP), mean arterial pressure, diastolic BP, heart rate (HR), and pulse pressure were similar in WT and TNFR1(-/-) mice. Infusion of ANG II for 7 days elevated SBP to a greater extent in TNFR1(-/-) compared with WT mice; pulse pressure was also elevated in TNFR1(-/-). HR decreased in TNFR1(-/-) mice infused with ANG II, an effect prominent on day 1. Basal urinary albumin excretion was similar in WT and TNFR1(-/-) mice but was higher in TNFR1(-/-) in response to ANG II infusion. Water intake and urine volume were increased by ANG II infusion; this increase was higher in TNFR1(-/-) vs. WT mice, whereas body weight and food intake were unaffected. Baseline creatinine clearance (Ccr), urinary sodium excretion, and fractional excretion of sodium (FE(Na)%) were similar in vehicle-treated WT and TNFR1(-/-) mice. ANG II infusion for 7 days increased Ccr and filtered load of sodium in TNFR1(-/-) but not WT mice, whereas it elicited an increase in FE(Na)% and urinary sodium excretion in WT but not TNFR1(-/-) mice. ANG II also inhibited renal TNFR1 mRNA accumulation while increasing that of TNFR2. These findings indicate deletion of TNFR1 is associated with an exacerbated SBP response, decrease in HR, and altered renal function in ANG II-dependent hypertension.
Authors:
Chun Cheng Andy Chen; Paulina L Pedraza; Shoujin Hao; Charles T Stier; Nicholas R Ferreri
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-08-25
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  299     ISSN:  1522-1466     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-04     Completed Date:  2010-12-02     Revised Date:  2011-11-01    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F1141-50     Citation Subset:  IM    
Affiliation:
Dept. of Pharmacology, New York Medical College, Valhalla, NY 10595, USA.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / pharmacology*
Animals
Blood Pressure / physiology*
Body Weight / physiology
Eating / physiology
Heart Rate / drug effects,  physiology
Kidney / drug effects*
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
RNA, Messenger / biosynthesis,  genetics
Receptors, Tumor Necrosis Factor, Type I / deficiency*,  genetics*
Renal Circulation / drug effects
Telemetry
Tumor Necrosis Factor-alpha / biosynthesis,  genetics
Vasoconstrictor Agents / pharmacology*
Grant Support
ID/Acronym/Agency:
HL-085439/HL/NHLBI NIH HHS; HL-34300/HL/NHLBI NIH HHS; R01 HL085439-03/HL/NHLBI NIH HHS; R01 HL085439-04/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/RNA, Messenger; 0/Receptors, Tumor Necrosis Factor, Type I; 0/Tumor Necrosis Factor-alpha; 0/Vasoconstrictor Agents; 11128-99-7/Angiotensin II

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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