Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1989-5-2
pubmed:abstractText
The efflux of 36C1 from perifused rat lenses consisted of two components: a fast (extracellular) component and a slow (cellular) component. The 36C1 efflux rate constant of the cellular component was 5.7 X 10(-3) min-1. The 36C1- efflux was sensitive to changes in lens potential induced by treatment with high-K+ solutions. The decrease in the 36C1- efflux rate constant caused by high-K+ solutions was consistent with the Goldman model, indicating that, under normal conditions, the majority of the 36C1 efflux is by diffusion. The 36C1- efflux rate constant corresponds to a C1 permeability of 1.3 X 10(8) ms 1. The C1- channel inhibitor anthracene-9-carboxylate (A-9-C), however, caused a relatively small reduction in the efflux rate constant. The anion-exchange inhibitor 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonate (SITS) has little effect on the 36C1 efflux under control conditions. Intracellular acidification, induced by pre-treatment with NH1+, leads to a rapid stimulation of 36C1- efflux. This increased 36C1- efflux is blocked by SITS. Thus, it appears that at low intracellular pH (pH), a normally quiescent, SITS-sensitive, anion-exchange mechanism is activated. The possible role of this exchange mechanism in regulating pH, is discussed.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0144-8757
pubmed:author
pubmed:issnType
Print
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
941-9
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Efflux of chloride from the rat lens: influence of membrane potential and intracellular acidification.
pubmed:affiliation
School of Biological Sciences, University of East Anglia, Norwich.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't