| Blood pressure and renal blow flow responses in heme oxygenase-2 knockout mice. | |
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MedLine Citation:
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PMID: 19846746 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Heme oxygenase (HO) is the enzyme responsible for the breakdown of heme-generating carbon monoxide (CO) and biliverdin in this process. HO-2 is the constitutively expressed isoform in most tissues, such as the kidney and vasculature. CO generated by HO is believed to be an important vasodilator in the renal circulation along with another gas, nitric oxide (NO). To determine the importance of HO-2 in the regulation of blood pressure and renal blood flow (RBF), we treated HO-2 knockout (KO) mice chronically with either ANG II or N(G)-nitroarginine methyl ester (l-NAME). Basal blood pressures were not different between wild-type (WT), heterozygous (HET), or KO mice and averaged 113 +/- 3 vs. 115 +/- 2 vs. 116 +/- 2 mmHg. Similar increases in blood pressure to chronic ANG II as well as l-NAME treatment were observed in all groups with blood pressures increasing an average of 30 mmHg in response to ANG II and 15 mmHg in response to l-NAME. Basal RBFs were not different between the groups averaging 6.0 +/- 0.5 (n = 6) vs. 4.8 +/- 0.6 (n = 10) vs. 5.8 +/- 0.7 (n = 6) ml*min(-1)*g(-1) kidney weight in WT, HET, and KO mice. HO-2 KO and HET mice exhibited an attenuated decrease in RBF in response to acute administration of ANG II, while no differences were observed with l-NAME. Our data indicate that blood pressure and RBF responses to increased ANG II or inhibition of nitric oxide are not significantly enhanced in HO-2 KO mice. |
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Authors:
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David E Stec; Trinity Vera; Megan V Storm; Gerald R McLemore; Michael J Ryan |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2009-10-21 |
Journal Detail:
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Title: American journal of physiology. Regulatory, integrative and comparative physiology Volume: 297 ISSN: 1522-1490 ISO Abbreviation: Am. J. Physiol. Regul. Integr. Comp. Physiol. Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2009-11-25 Completed Date: 2009-12-11 Revised Date: 2011-03-03 |
Medline Journal Info:
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Nlm Unique ID: 100901230 Medline TA: Am J Physiol Regul Integr Comp Physiol Country: United States |
Other Details:
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Languages: eng Pagination: R1822-8 Citation Subset: IM |
Affiliation:
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Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi 39215, USA. dstec@physiology.umsmed.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Administration, Oral Angiotensin II / administration & dosage Animals Blood Pressure* Cardiomegaly / enzymology, genetics, physiopathology Disease Models, Animal Female Heme Oxygenase (Decyclizing) / deficiency*, genetics Hypertension / chemically induced, enzymology*, genetics, physiopathology Infusion Pumps, Implantable Infusions, Subcutaneous Kidney / blood supply* Male Mice Mice, Inbred C57BL Mice, Knockout NG-Nitroarginine Methyl Ester / administration & dosage Nitric Oxide Synthase / antagonists & inhibitors, metabolism Renal Circulation* Vascular Resistance Vasoconstriction |
| Grant Support | |
ID/Acronym/Agency:
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HL-085907/HL/NHLBI NIH HHS; HL-085907-S1/HL/NHLBI NIH HHS; HL-088421/HL/NHLBI NIH HHS; HL-088421-S1/HL/NHLBI NIH HHS; HL-092284/HL/NHLBI NIH HHS; P01-HL-5197/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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11128-99-7/Angiotensin II; 50903-99-6/NG-Nitroarginine Methyl Ester; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.99.3/Heme Oxygenase (Decyclizing); EC 1.14.99.3/heme oxygenase-2 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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