Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-9-26
pubmed:abstractText
1. Single cell photometry and whole-cell patch clamp recording were used to study caffeine-induced intracellular Ca2+ signals and membrane currents, respectively, in endothelial cells freshly dissociated from rabbit aorta. 2. Caffeine (5 mM) evoked a transient increase in [Ca2+]i in fura-2-loaded endothelial cells. Pretreatment of cells with 10 microM ryanodine did not alter resting [Ca2+]i but irreversibly inhibited the caffeine-induced rise in [Ca2+]i. The caffeine-induced increase in [Ca2+]i was not attenuated by the removal of extracellular Ca2+ and did not stimulate the rate of Mn2+ quench of fura-2 fluorescence. 3. Bath application of caffeine evoked a dose- and voltage-dependent outward current. The rate of onset and amplitude of the caffeine-evoked outward current increased with higher caffeine concentrations and membrane depolarization. The relationship between caffeine-evoked current amplitude and membrane potential was non linear, suggesting that the channels underlying the current are voltage-sensitive. 4. In the absence of extracellular Ca2+, the amplitude of the caffeine-evoked outward current was reduced by approximately 50% but the duration of the current was prolonged compared to that observed in the presence of external Ca2+. Ca(2+)-free external solutions produced an unexpected increase in both the frequency and amplitude of spontaneous transient outward currents (STOCs). 5. Inclusion of heparin (10 micrograms ml-1) in the patch pipette abolished the acetylcholine (ACh)-induced outward current but failed to inhibit either STOCs or the caffeine-evoked outward current in native endothelial cells. In the absence of extracellular Ca2+, heparin did not affect either STOCs or the caffeine-induced outward current. 6. Externally applied tetraethylammonium ions (TEA, 3-10mM) reversibly inhibited unitary Ca2+-activated K+ currents and STOCs in endothelial cells but failed to inhibit completely the outward current evoked by 20 mM caffeine.7. Bath application of 0.1 mM zinc ion (Zn2+), a chloride channel blocker, did not affect unitary currents or STOCs but reduced the amplitude of the caffeine-evoked current by >75% compared to control. Replacement of extracellular NaCl with Na gluconate also reduced the amplitude of the caffeine-induced outward current. Bath application of 0.1 mM Zn2+ and 10 mM TEA completely blocked the caffeine-evoked outward current in endothelial cells.8. Caffeine-induced Ca2+ release from intracellular stores evokes a transient rise in [Ca2+1, which is correlated with a large, transient outward current. The ionic dependence and inhibition of the caffeine sensitive current by TEA and Zn2+ suggests that Ca2+-activated K+ and Cl- conductances contribute to the caffeine response in rabbit aortic endothelial cells.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-1291681, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-1318033, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-1382265, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-1484364, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-1697946, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-1720891, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-1904293, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-2177344, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-2348402, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-2385008, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-2442353, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-2452017, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-2453021, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-2541679, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-2585296, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-2798038, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-3064851, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-3110148, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-3136153, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-3136667, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-3194169, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-3223917, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-3838314, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-6040156, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-6270629, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-7913485, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-8010945, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-8036248, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-8092278, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-8261589, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-8380279, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-8380362, http://linkedlifedata.com/resource/pubmed/commentcorrection/7647967-8383430
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0007-1188
pubmed:author
pubmed:issnType
Print
pubmed:volume
115
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
133-41
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Caffeine-evoked, calcium-sensitive membrane currents in rabbit aortic endothelial cells.
pubmed:affiliation
Department of Molecular & Cellular Pharmacology, University of Miami School of Medicine, FL 33101, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.