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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Pt 1
pubmed:dateCreated
1986-3-28
pubmed:abstractText
In response to infection, neutrophils undergo a metabolic burst associated with a marked increase in acid generation. However, cytoplasmic pH (pHi) remains normal or even becomes slightly alkaline. Regulation of pHi is due, at least in part, to a Na+-H+ exchange mechanism. The basic properties of this antiport were investigated in human blood neutrophils using fluorescein derivatives as pHi indicators and by means of electronic cell sizing. Addition of external Na+ (Na+o) to acid-loaded cells resulted in intracellular alkalinization due to transmembrane H+ (equivalent) flux. The alkalinization was associated with Na+ uptake, and both processes were blocked by amiloride, suggesting Na+-H+ countertransport. The rate of amiloride-sensitive H+ efflux could be calculated from the rate of change of pHi, using a buffering power of 28 mmol X l-1 X pH unit-1, determined by titration with NH+4 or propionate-. The rate of Na+o-H+i exchange was a saturable function of Na+o (apparent Km = 73 mM). Forward (Na+o-H+i) exchange was inhibited by elevating external [H+] or internal [Na+] and competitively by amiloride (apparent Ki = 24 microM). The antiport was virtually inactive in unstimulated cells at pHi greater than or equal to 7.2 but was markedly stimulated by cytoplasmic acidification. This behavior is consistent with a role in pHi homeostasis. The possible mechanisms of stimulation of Na+-H+ countertransport in resting and activated neutrophils are discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
250
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C283-91
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
Characterization of the amiloride-sensitive Na+-H+ antiport of human neutrophils.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't