| pubmed-article:11847186 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11847186 | lifeskim:mentions | umls-concept:C0020538 | lld:lifeskim |
| pubmed-article:11847186 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
| pubmed-article:11847186 | lifeskim:mentions | umls-concept:C0005823 | lld:lifeskim |
| pubmed-article:11847186 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:11847186 | lifeskim:mentions | umls-concept:C1333402 | lld:lifeskim |
| pubmed-article:11847186 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:11847186 | pubmed:dateCreated | 2002-2-15 | lld:pubmed |
| pubmed-article:11847186 | pubmed:abstractText | ACE plays an important role in the regulation of arterial pressure; however, a linear relationship between ACE expression and arterial pressure has not been demonstrated. The present study employed telemetric monitoring in female transgenic mice to determine the influence of partial and complete deletion of the ACE gene on basal arterial pressure and arterial pressure responses to a high-NaCl diet. On the basal NaCl diet, 24-hour mean arterial pressure was significantly correlated with the number of functional copies of the ACE gene; ie, arterial pressure was lowest in 0-copy (80 +/- 1 mm Hg), intermediate in 1-copy (100 +/- 1 mm Hg), and highest in 2-copy (113 +/- 1 mm Hg) ACE mice. The high-NaCl diet significantly increased mean arterial pressure in 0-copy (99 +/- 1 mm Hg) and 1-copy (108 +/- 1 mm Hg) mice but not in 2-copy mice (114 +/- 1 mm Hg). These results demonstrate a copy-dependent relationship between ACE gene expression and both basal arterial pressure and arterial pressure responses to a high-NaCl diet, suggesting that either partial or complete reduction in the ACE gene can alter arterial pressure. | lld:pubmed |
| pubmed-article:11847186 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11847186 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11847186 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11847186 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11847186 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11847186 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11847186 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11847186 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:11847186 | pubmed:issn | 1524-4563 | lld:pubmed |
| pubmed-article:11847186 | pubmed:author | pubmed-author:OparilSuzanne... | lld:pubmed |
| pubmed-article:11847186 | pubmed:author | pubmed-author:ChenYiu-FaiYF | lld:pubmed |
| pubmed-article:11847186 | pubmed:author | pubmed-author:CarlsonScott... | lld:pubmed |
| pubmed-article:11847186 | pubmed:author | pubmed-author:WyssJ... | lld:pubmed |
| pubmed-article:11847186 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:11847186 | pubmed:volume | 39 | lld:pubmed |
| pubmed-article:11847186 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11847186 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11847186 | pubmed:pagination | 214-8 | lld:pubmed |
| pubmed-article:11847186 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:meshHeading | pubmed-meshheading:11847186... | lld:pubmed |
| pubmed-article:11847186 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11847186 | pubmed:articleTitle | Blood pressure and NaCl-sensitive hypertension are influenced by angiotensin-converting enzyme gene expression in transgenic mice. | lld:pubmed |
| pubmed-article:11847186 | pubmed:affiliation | Vascular Biology and Hypertension Program of the Department of Medicine, University of Alabama at Birmingham, USA. | lld:pubmed |
| pubmed-article:11847186 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11847186 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| entrez-gene:11421 | entrezgene:pubmed | pubmed-article:11847186 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:11847186 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:11847186 | lld:pubmed |
