Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1993-3-29
pubmed:abstractText
1. Using microfluorimetry, intracellular pH, buffering capacity and intracellular pH recovery from intracellular acidosis were determined in isolated adult rat ventricular myocytes, in buffers with and without HCO3-. 2. In nominally HCO3(-)-free media, the intracellular pH was higher than in HCO3(-)-containing media. Buffering capacity at resting intracellular pH and at a pH of about 6.3 was also lower in HCO3(-)-free media. 3. In HCO3(-)-free media, recovery from an acid load after an NH4Cl prepulse was almost completely inhibited by the Na+/H+ antiport activity specific inhibitor ethylisopropyl amiloride. However, in the presence of HCO3-, H+ efflux rate was enhanced, and ethylisopropyl amiloride led to only partial inhibition of H+ efflux. Complete inhibition was achieved only with further addition of the anion-transport inhibitor 4,4'-di-isothiocyanatostilbene-2,2'-disulphonate. 4. Thus, in adult rat ventricular myocytes, recovery from intracellular acidosis in the absence of HCO3- was almost wholly due to Na+/H+ antiport activity. In the more physiological situation with HCO3- present, a third of the recovery from an intracellular acid load was attributed to an additional external Na(+)-dependent di-isothiocyanatostilbene-disulphonate-sensitive H+ efflux.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0143-5221
pubmed:author
pubmed:issnType
Print
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
133-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Intracellular pH regulation in isolated myocytes from adult rat heart in HCO3(-)-containing and HCO3(-)-free media.
pubmed:affiliation
Department of Pharmacology, Leicester Royal Infirmary, U.K.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't