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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0030685,
umls-concept:C0036226,
umls-concept:C0085979,
umls-concept:C0391871,
umls-concept:C0439831,
umls-concept:C0521116,
umls-concept:C0596235,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1963578,
umls-concept:C2004454,
umls-concept:C2339371
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pubmed:issue |
1
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pubmed:dateCreated |
1995-1-26
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pubmed:abstractText |
We have investigated the modulation of the L-type Ca2+ channel by Ca2+ released from the sarcoplasmic reticulum (SR) in single guinea pig ventricular myocytes under whole-cell voltage clamp. [Ca2+]i was monitored by fura 2. By use of impermeant monovalent cations in intracellular and extracellular solutions, the current through Na+ channels, K+ channels, nonspecific cation channels, and the Na+-Ca2+ exchanger was effectively blocked. By altering the amount of Ca2+ loading of the SR, the time course of the Ca2+ current (ICa) could be studied during various amplitudes of Ca2+ release. In the presence of a large Ca2+ release, fast inhibition of ICa occurred, whereas on relaxation of [Ca2+]i, fast recovery was observed. The time course of this transient inhibition of ICa reflected the time course of [Ca2+]i. However, the inhibition seen in the first 50 ms, ie, the time of net Ca2+ release from the SR, exceeded the inhibition observed later during the pulse, suggesting the existence of a higher [Ca2+] near the channel during this time. Transient inhibition of ICa during Ca2+ release was observed to a similar degree at all potentials. It could still be observed in the presence of intracellular ATP-gamma-S and of cAMP. Therefore, we conclude that the modulation of ICa by Ca2+ release from the SR is not related to dephosphorylation. It could be related to a reduction in the driving force and to a direct inhibition of the channel by [Ca2+]i. The observation that the degree of inhibition does not depend on membrane potential suggests that the Ca2+ binding site for this modulation is located outside the pore.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0009-7330
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
76
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
102-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8001267-Animals,
pubmed-meshheading:8001267-Calcium,
pubmed-meshheading:8001267-Calcium Channels,
pubmed-meshheading:8001267-Fura-2,
pubmed-meshheading:8001267-Guinea Pigs,
pubmed-meshheading:8001267-Heart Ventricles,
pubmed-meshheading:8001267-Myocardium,
pubmed-meshheading:8001267-Phosphorylation,
pubmed-meshheading:8001267-Sarcoplasmic Reticulum
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pubmed:year |
1995
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pubmed:articleTitle |
Inhibition and rapid recovery of Ca2+ current during Ca2+ release from sarcoplasmic reticulum in guinea pig ventricular myocytes.
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pubmed:affiliation |
Laboratory of Physiology, University of Leuven, Belgium.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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