| Enhanced heme oxygenase-mediated coronary vasodilation in Dahl salt-sensitive hypertension. | |
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MedLine Citation:
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PMID: 14700508 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Cardiovascular tissues express heme oxygenase (HO), which metabolizes heme to form carbon monoxide (CO). Carbon monoxide promotes relaxation of coronary vascular smooth muscle. Increased HO-1 expression provides cardioprotection during certain pathologic conditions. On a high salt (HS) diet Dahl salt-sensitive (DS) rats develop hypertension that is accompanied by left ventricular hypertrophy, whereas Dahl salt-resistant rats (DR) do not. This study tests the hypothesis that cardiac HO-1 expression is increased in DS rats with salt-induced hypertension and provides cardioprotection by promoting coronary vasodilation. METHODS: Male DS and DR rats were placed on a HS (8% NaCl) or low salt (LS, 0.3% NaCl) diet for 4 weeks. Cardiac HO isoform expression were determined by immunohistochemistry. Experiments used isolated paced Langendorff-hearts perfused at a constant flow. Changes in coronary perfusion pressure and left ventricular contractility (dP/dt(max)) were measured in response to an inhibitor of HO, chromium mesoporphyrin (CrMP). RESULTS: With respect to the LS group, DS rats on HS diet showed elevated mean arterial pressure and increased heart weight. Coronary arterial HO-1 immunostaining was enhanced in HS rats, but HO-2 staining was similar in both groups. In isolated Langendorff-hearts the HO inhibitor CrMP increased coronary perfusion pressure and calculated coronary resistance, and decreased left ventricular contractility (dP/dt(max)) in both groups, but the response was exaggerated in HS rat hearts. In the DR strain, HS diet did not augment CrMP responses and had no effect on any of the parameters measured with respect to the LS diet. CONCLUSIONS: These findings suggest that coronary HO-1 expression is increased to promote enhanced coronary vasodilation in DS rats with salt-induced hypertension. |
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Authors:
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Robert A Johnson; Federico J Teran; William Durante; Kelly J Peyton; Fruzsina K Johnson |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: American journal of hypertension Volume: 17 ISSN: 0895-7061 ISO Abbreviation: Am. J. Hypertens. Publication Date: 2004 Jan |
Date Detail:
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Created Date: 2003-12-31 Completed Date: 2004-08-12 Revised Date: 2009-02-24 |
Medline Journal Info:
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Nlm Unique ID: 8803676 Medline TA: Am J Hypertens Country: United States |
Other Details:
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Languages: eng Pagination: 25-30 Citation Subset: IM |
Affiliation:
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Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana 70112, USA. RobertJ393@aol.com |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Coronary Circulation / physiology* Disease Models, Animal Heart Rate Heme Oxygenase (Decyclizing) / metabolism* Humans Hypertension / etiology, physiopathology* Immunohistochemistry Male Myocardium / metabolism Rats Rats, Inbred Dahl Sodium, Dietary / adverse effects* Vasodilation / physiology* |
| Grant Support | |
ID/Acronym/Agency:
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P20 RR017659/RR/NCRR NIH HHS; R01 HL59976/HL/NHLBI NIH HHS; R01 HL64577/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Sodium, Dietary; EC 1.14.99.3/Heme Oxygenase (Decyclizing) |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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