Document Detail

Pressure-overload deinduction of human alpha 2 Na,K-ATPase gene expression in transgenic rats.
MedLine Citation:
PMID:  9040446     Owner:  NLM     Status:  MEDLINE    
The early and sustained deinduction of alpha 2 Na,K-ATPase gene expression in both cardiac left ventricle and aorta in various pressure-overload rat models and in hypertrophied human heart suggests a common transcriptional pressure response mechanism to pressure overload in both rats and humans. To test this hypothesis, we developed transgenic rat lines expressing the chloramphenicol acetyltransferase reporter gene regulated by the human alpha 2 Na,K-ATPase (-798 to +67) regulatory region, H alpha 2-CAT. Analysis of two homozygous transgenic rat lines revealed (1) parallel tissue-specific regulation of the H alpha 2-CAT transgene and rat alpha 2 Na,K-ATPase gene and (2) parallel load-induced deinduction of both cardiac and vascular (aortic) H alpha 2-CAT transgene and rat alpha 2 Na,K-ATPase gene expression in a 3-day model of induced pressure overload. Cardiac H alpha 2-CAT deinduction was detected at a systolic pressure greater than or equal to 150 mm Hg and correlated with the degree of systolic pressure elevation (r = .82, P < .0001). The data suggest a systolic pressure gradient-dependent coordinate pressure-overload transcriptional response mechanism in the heart and aorta, with one of its target genes being the alpha 2 Na,K-ATPase gene in both humans and rats.
N Ruiz-Opazo; X H Xiang; V L Herrera
Related Documents :
1707326 - Chronic nerve growth factor treatment of normotensive rats.
6685486 - Cardiovascular effects of a new antihypertensive agent in several species.
2071246 - Cyclosporine-associated reduction in systolic myocardial function in the rat.
25243656 - High pressure homogenization and two-phased anaerobic digestion for enhanced biogas con...
6021206 - Comparison of effects of deoxycorticosterone and dexamethasone on cardiovascular respon...
12055446 - How and why to do pressure ulcer risk assessment.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Hypertension     Volume:  29     ISSN:  0194-911X     ISO Abbreviation:  Hypertension     Publication Date:  1997 Feb 
Date Detail:
Created Date:  1997-03-13     Completed Date:  1997-03-13     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  606-12     Citation Subset:  IM    
Section of Molecular Genetics, Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston (Mass) University School of Medicine 02118, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Angiotensin II / pharmacology
Animals, Genetically Modified
Aorta / metabolism
Blood Pressure / drug effects
Brain / metabolism
Cells, Cultured
Chloramphenicol O-Acetyltransferase
Down-Regulation / genetics*
Muscle, Skeletal / metabolism
Myocardium / metabolism
Rats, Sprague-Dawley
Sodium-Potassium-Exchanging ATPase / genetics*,  metabolism*
Stress, Physiological / genetics*
Grant Support
Reg. No./Substance:
11128-99-7/Angiotensin II; EC O-Acetyltransferase; EC ATPase

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

Previous Document:  Brain 'ouabain' in the median preoptic nucleus mediates sodium-sensitive hypertension in spontaneous...
Next Document:  Spontaneously hypertensive rat Y chromosome increases indexes of sympathetic nervous system activity...