Linked Life Data

9633914

Source:http://linkedlifedata.com/resource/pubmed/id/9633914

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1998-7-2
pubmed:abstractText
Recently, we found that vacuolar proton ATPase (VPATPase) operates in cardiomyocytes as a complementary proton-extruding mechanism. Its activity was increased by preconditioning with resultant attenuation of intracellular acidification during ischemia. In this study, we examined whether VPATPase-mediated proton efflux during metabolic inhibition/recovery may spare Na+ overload via Na+-H+ exchange, attenuate Na+-Ca2+ exchange, and decrease apoptosis. Neonatal rat cardiomyocytes were subjected to 2- to 3-hour metabolic inhibition with cyanide and 2-deoxyglucose and 24-hour recovery. The effect of VPATPase inhibition by 50 nmol/L bafilomycin A1 on apoptosis, pHi, and [Ca2+]i was studied by flow cytometry with propidium iodide, seminaphthorhodafluor (SNARF)-1-AM, and indo-1-AM staining, respectively. VPATPase inhibition increased the amount of apoptosis measured after 24 hours of recovery and abrogated the protective effect of inhibition of Na+-H+ exchange by (5-N-ethyl-N-isopropyl)amiloride (EIPA). Dual blockade of VPATPase and Na+-H+ exchange was additive in effect with EIPA on pHi during metabolic inhibition/recovery and recovery from the acid challenge with sodium propionate. VPATPase blockade increased the rate of accumulation of intracellular Ca2+ at the beginning of metabolic inhibition and abrogated the delaying effect of EIPA on intracellular Ca2+ accumulation. These results indicate that VPATPase plays an important accessory role in cardiomyocyte protection by reducing acidosis and Na+-H+ exchange-induced Ca2+ overload.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0009-7330
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
82
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1139-44
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:9633914-Amiloride, pubmed-meshheading:9633914-Animals, pubmed-meshheading:9633914-Animals, Newborn, pubmed-meshheading:9633914-Anti-Arrhythmia Agents, pubmed-meshheading:9633914-Anti-Bacterial Agents, pubmed-meshheading:9633914-Apoptosis, pubmed-meshheading:9633914-Calcium, pubmed-meshheading:9633914-Cells, Cultured, pubmed-meshheading:9633914-Dose-Response Relationship, Drug, pubmed-meshheading:9633914-Energy Metabolism, pubmed-meshheading:9633914-Enzyme Inhibitors, pubmed-meshheading:9633914-Hydrogen-Ion Concentration, pubmed-meshheading:9633914-Macrolides, pubmed-meshheading:9633914-Muscle Fibers, Skeletal, pubmed-meshheading:9633914-Myocardium, pubmed-meshheading:9633914-Proton-Translocating ATPases, pubmed-meshheading:9633914-Rats, pubmed-meshheading:9633914-Rats, Sprague-Dawley, pubmed-meshheading:9633914-Sodium-Calcium Exchanger, pubmed-meshheading:9633914-Sodium-Hydrogen Antiporter, pubmed-meshheading:9633914-Vacuoles
pubmed:year
1998
pubmed:articleTitle
Effect of vacuolar proton ATPase on pHi, Ca2+, and apoptosis in neonatal cardiomyocytes during metabolic inhibition/recovery.
pubmed:affiliation
Research Service, Veterans Affairs San Diego Healthcare System, University of California, San Diego, School of Medicine, 92161, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't