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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1995-12-22
pubmed:abstractText
Transient inward currents (Iti) during oscillations of intracellular [Ca2+] ([Ca2+]i) in ventricular myocytes have been ascribed to Na/Ca exchange. We have investigated whether other Ca2+-dependent membrane currents contribute to Iti in single guinea-pig ventricular myocytes, by examining membrane currents during [Ca2+]i oscillations and during caffeine-induced Ca2+ release from the sarcoplasmic reticulum in the absence of Na+. Membrane currents were recorded during whole-cell voltage clamp and [Ca2+]i measured simultaneously with fura-2. In the absence of Na/Ca exchange, i.e., with Li+, Cs+ or N-methyl-D-glucamine (NMDG+) substituted for Na+, the cell could be loaded with Ca2+ by repetitive depolarizations to +10 mV, resulting in spontaneous [Ca2+]i oscillations. During these oscillations, no inward currents were seen, but instead spontaneous Ca2+ release was accompanied by a shift of the membrane current in the outward direction at potentials between -40 mV and +60 mV. This [Ca2+]i-dependent outward current shift was not abolished when NMDG+ was substituted for internal monovalent cations, nor was it sensitive to substitution of external Cl-. It was however, sensitive to the blockade of ICa by verapamil. These results suggest that the transient outward current shift observed during spontaneous Ca2+ release represents [Ca2+]i-dependent transient inhibition of ICa. Similarly, during the [Ca2+]i transients induced by brief caffeine (10 mM) applications, we could not detect membrane currents attributable to a Ca2+-activated nonselective cation channel, or to a Ca2+-activated Cl- channel; however, transient Ca2+-dependent inhibition of ICa was again observed. We conclude that neither the Ca2+-activated nonselective cation channel nor the Ca2+-activated Cl- channel contribute significantly to the membrane currents during spontaneous [Ca2+]i oscillations in guinea-pig ventricular myocytes. However, in the voltage range between -40 mV and +60 mV Ca2+-dependent transient inhibition of ICa will contribute to the oscillations of the membrane current.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
430
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
871-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:7478945-Animals, pubmed-meshheading:7478945-Caffeine, pubmed-meshheading:7478945-Calcium, pubmed-meshheading:7478945-Calcium Channel Blockers, pubmed-meshheading:7478945-Calcium Channels, pubmed-meshheading:7478945-Carrier Proteins, pubmed-meshheading:7478945-Cations, pubmed-meshheading:7478945-Cell Membrane, pubmed-meshheading:7478945-Chloride Channels, pubmed-meshheading:7478945-Guinea Pigs, pubmed-meshheading:7478945-Heart, pubmed-meshheading:7478945-Heart Ventricles, pubmed-meshheading:7478945-Membrane Potentials, pubmed-meshheading:7478945-Myocardial Contraction, pubmed-meshheading:7478945-Myocardium, pubmed-meshheading:7478945-Patch-Clamp Techniques, pubmed-meshheading:7478945-Sodium, pubmed-meshheading:7478945-Sodium-Calcium Exchanger, pubmed-meshheading:7478945-Verapamil
pubmed:year
1995
pubmed:articleTitle
[Ca2+]i-dependent membrane currents in guinea-pig ventricular cells in the absence of Na/Ca exchange.
pubmed:affiliation
Laboratory of physiology, Katholieke Universiteit Leuven, Campus Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't