Linked Life Data

3017962

Source:http://linkedlifedata.com/resource/pubmed/id/3017962

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
26
pubmed:dateCreated
1986-10-17
pubmed:abstractText
Using the pH-sensitive absorbance of 5 (and 6)-carboxy-4',5'- dimethylfluorescein, we investigated the regulation of cytoplasmic pH (pHi) in monkey kidney epithelial cells (BSC-1). In the absence of HCO3-, pHi is 7.15 +/- 0.1, which is not significantly different from pHi in 28 mM HCO3-, 5% CO2 (7.21 +/- 0.07). After an acid load, the cells regulate pHi in the absence of HCO3- by a Na+ (or Li+)-dependent, amiloride-inhibitable mechanism (indicative of Na+/H+ antiport). In 28 mM HCO3-, while still dependent on Na+, this regulation is only blocked in part by 1 mM amiloride. A partial block is also observed with 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) (1 mM). With cells pretreated with DIDS, 1 mM amiloride nearly totally inhibits this regulation. Cl- had no effect on pHi regulation in the acidic range. In HCO3(-)-free saline, Na+ removal leads to an amiloride-insensitive acidification, which is dependent on Ca2+. In 28 mM HCO3-, Na+ (and Ca2+) removal led to a pronounced reversible and DIDS-sensitive acidification. When HCO3- was lowered from 46 to 10 mM at constant pCO2 (5%), pHi dropped by a DIDS-sensitive mechanism. Identical changes in pHo (7.6 to 6.9) in the nominal absence of HCO3- led to smaller changes of pHi. In the presence but not in the absence of HCO3-, removal of Cl- led to a DIDS-sensitive alkalinization. This was also observed in the nominal absence of Na+, which leads to a sustained acidification. It is concluded that in nominally bicarbonate-free saline, the amiloride-sensitive Na+/H+ antiport is the predominant mechanism of pHi regulation at acidic pHi, while being relatively inactive at physiological values of pHi. In bicarbonate saline, two other mechanisms effect pHi regulation: a DIDS-sensitive Na+-HCO3- symport, which contributes to cytoplasmic alkalinization, and a DIDS-sensitive Cl-/HCO3- exchange, which is apparently independent of Na+.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
261
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
12120-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:3017962-4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid, pubmed-meshheading:3017962-4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid, pubmed-meshheading:3017962-Amiloride, pubmed-meshheading:3017962-Animals, pubmed-meshheading:3017962-Bicarbonates, pubmed-meshheading:3017962-Body Fluids, pubmed-meshheading:3017962-Carrier Proteins, pubmed-meshheading:3017962-Chloride-Bicarbonate Antiporters, pubmed-meshheading:3017962-Chlorides, pubmed-meshheading:3017962-Epithelial Cells, pubmed-meshheading:3017962-Epithelium, pubmed-meshheading:3017962-Haplorhini, pubmed-meshheading:3017962-Hydrogen-Ion Concentration, pubmed-meshheading:3017962-Intracellular Fluid, pubmed-meshheading:3017962-Kidney, pubmed-meshheading:3017962-Sodium-Bicarbonate Symporters, pubmed-meshheading:3017962-Sodium-Hydrogen Antiporter
pubmed:year
1986
pubmed:articleTitle
The regulation of intracellular pH in monkey kidney epithelial cells (BSC-1). Roles of Na+/H+ antiport, Na+-HCO3(-)-(NaCO3-) symport, and Cl-/HCO3- exchange.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't