Linked Life Data

17075028

Source:http://linkedlifedata.com/resource/pubmed/id/17075028

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-12-22
pubmed:abstractText
Recent studies have demonstrated that inhibition of renal medullary heme oxygenase (HO) activity and carbon monoxide (CO) significantly decreases renal medullary blood flow and sodium excretion. Given the crucial role of renal medullary blood flow in the control of pressure natriuresis, the present study was designed to determine whether renal medullary HO activity and resulting CO production participate in the regulation of pressure natriuresis and thereby the long-term control of arterial blood pressure. In anesthetized Sprague-Dawley rats, increases in renal perfusion pressure induced significant elevations of CO concentrations in the renal medulla. Renal medullary infusion of chromium mesoporphyrin (CrMP), an inhibitor of HO activity, remarkably inhibited HO activity and the renal perfusion pressure-dependent increases in CO levels in the renal medulla and significantly blunted pressure natriuresis. In conscious Sprague-Dawley rats, continuous infusion of CrMP into the renal medulla significantly increased mean arterial pressure (129+/-2.5 mm Hg in CrMP group versus 118+/-1.6 mm Hg in vehicle group) when animals were fed a normal salt diet (1% NaCl). After rats were switched to a high-salt diet (8% NaCl) for 10 days, CrMP-treated animals exhibited further increases in mean arterial pressure compared with CrMP-treated animals that were kept on normal salt diet (152+/-4.1 versus 130+/-4.2 mm Hg). These results suggest that renal medullary HO activity plays a crucial role in the control of pressure natriuresis and arterial blood pressure and that impairment of this HO/CO-mediated antihypertensive mechanism in the renal medulla may result in the development of hypertension.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
148-54
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed-meshheading:17075028-Animals, pubmed-meshheading:17075028-Blood Pressure, pubmed-meshheading:17075028-Carbon Monoxide, pubmed-meshheading:17075028-Dose-Response Relationship, Drug, pubmed-meshheading:17075028-Drug Administration Schedule, pubmed-meshheading:17075028-Enzyme Inhibitors, pubmed-meshheading:17075028-Heme Oxygenase (Decyclizing), pubmed-meshheading:17075028-Kidney, pubmed-meshheading:17075028-Kidney Medulla, pubmed-meshheading:17075028-Male, pubmed-meshheading:17075028-Mesoporphyrins, pubmed-meshheading:17075028-Natriuresis, pubmed-meshheading:17075028-Nitric Oxide, pubmed-meshheading:17075028-Osmolar Concentration, pubmed-meshheading:17075028-RNA, Messenger, pubmed-meshheading:17075028-Rats, pubmed-meshheading:17075028-Rats, Sprague-Dawley, pubmed-meshheading:17075028-Sodium Chloride, Dietary
pubmed:year
2007
pubmed:articleTitle
Role of renal medullary heme oxygenase in the regulation of pressure natriuresis and arterial blood pressure.
pubmed:affiliation
Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298, USA. nli@vcu.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural