Linked Life Data

17416604

Source:http://linkedlifedata.com/resource/pubmed/id/17416604

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-8-3
pubmed:abstractText
The Na(+)-HCO(3)(-) cotransporter (NBC) plays a key role in intracellular pH (pH(i)) regulation in normal ventricular muscle. However, the state of NBC in nonischemic hypertrophied hearts is unresolved. In this study, we examined functional and molecular properties of NBC in adult rat ventricular myocytes. The cells were enzymatically isolated from both normal and hypertrophied hearts. Ventricular hypertrophy was induced by pressure overload created by suprarenal abdominal aortic constriction of 50% for 7 wk. pH(i) was measured in single cells using the fluorescent pH indicator 2',7'-bis(2-carboxyethyl)5-(6)carboxyfluorescein. Real-time PCR analysis was used to quantitatively assess expression of NBC-encoding mRNA, including SLC4A4 (encoding electrogenic NBC, NBCe1) and SLC4A7 (electroneutral NBC, NBCn1). Our results demonstrate that: 1) mRNA levels of both the electrogenic NBCe1 (SLC4A4) and electroneutral NBCn1 (SLC4A7) forms of NBC were increased by aortic constriction, 2) the onset of NBC upregulation occurred within 3 days after constriction, 3) normal and hypertrophied ventricles displayed regional differences in NBC expression, 4) acid extrusion via NBC (J(NBC)) was increased significantly in hypertrophied myocytes, 5) although acid extrusion via Na(+)/H(+) exchange was also increased in hypertrophied myocytes, the relative enhancement of J(NBC) was larger, 6) membrane depolarization markedly increased J(NBC) in hypertrophied myocytes, and 7) losartan, an ANG II AT(1) receptor antagonist, significantly attenuated the upregulation of both NBCs induced by 3 wk of aortic constriction. Enhanced NBC activity during hypertrophic development provides a mechanism for intracellular Na(+) overload, which may render the ventricles more vulnerable to Ca(2+) overload during ischemia-reperfusion.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
293
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1254-64
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:17416604-Angiotensin II Type 1 Receptor Blockers, pubmed-meshheading:17416604-Animals, pubmed-meshheading:17416604-Aorta, Abdominal, pubmed-meshheading:17416604-Disease Models, Animal, pubmed-meshheading:17416604-Heart Ventricles, pubmed-meshheading:17416604-Hydrogen-Ion Concentration, pubmed-meshheading:17416604-Hypertension, pubmed-meshheading:17416604-Hypertrophy, Left Ventricular, pubmed-meshheading:17416604-Ligation, pubmed-meshheading:17416604-Losartan, pubmed-meshheading:17416604-Male, pubmed-meshheading:17416604-Membrane Potentials, pubmed-meshheading:17416604-Myocytes, Cardiac, pubmed-meshheading:17416604-RNA, Messenger, pubmed-meshheading:17416604-Rats, pubmed-meshheading:17416604-Rats, Wistar, pubmed-meshheading:17416604-Sodium-Bicarbonate Symporters, pubmed-meshheading:17416604-Sodium-Potassium-Exchanging ATPase, pubmed-meshheading:17416604-Time Factors, pubmed-meshheading:17416604-Transcription, Genetic, pubmed-meshheading:17416604-Up-Regulation
pubmed:year
2007
pubmed:articleTitle
Enhanced activity of ventricular Na+-HCO3- cotransport in pressure overload hypertrophy.
pubmed:affiliation
Department of Cardiology and Vascular Regenerative Medicine, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-8566, Japan. takuy24@koto.kpu-m.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural