Linked Life Data

17634415

Source:http://linkedlifedata.com/resource/pubmed/id/17634415

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-10-9
pubmed:abstractText
Spontaneous transient currents, due to activation of Ca(2+)-dependent K(+) and Cl(-) channels, occur in corpus cavernosum smooth muscle cells (CCSMC) of the penis. The Ca(2+) events responsible for triggering Ca(2+)-dependent Cl(-) channels have never been identified in vascular muscle. We used high-speed fluorescence imaging combined with patch-clamp electrophysiology to provide the first characterization of Ca(2+) events underlying these currents. Freshly isolated rat CCSMC loaded with fluo-4 exhibited localized, spontaneous elevations of intracellular Ca(2+) (Ca(2+) sparks) in 57% of cells. There was an average of 6.4 +/- 0.5 release sites/cell with a frequency of 0.9 +/- 1 Hz/cell and peak amplitude DeltaF/F(o) of 67 +/- 10%. We addressed the controversy of whether these events are mediated by ryanodine or inositol 1,4,5 trisphosphate (IP(3)) receptors. Caffeine caused either a global Ca(2+) rise at high concentrations or an increase in spark frequency at lower concentrations, whereas ryanodine dramatically reduced the amplitude and frequency of sparks. 2-Aminoethoxydiphenyl borate, an inhibitor of IP(3) receptors, had no effect on spark frequency. Combined imaging and electrophysiological recording revealed strong coupling between Ca(2+) sparks and biphasic transient currents, a relationship never before shown in vascular muscle. Moreover, spark frequency increased on depolarization, an effect abolished with the blockade of Ca(2+) channels, consistent with Ca(2+) influx regulating Ca(2+) release from stores. We establish for the first time that Ca(2+) sparks occur in CCSMC and arise from Ca(2+) release through ryanodine receptors. Moreover, the voltage dependence of spark frequency demonstrated here provides novel functional evidence for voltage-dependent Ca(2+) influx in CCSMC.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0363-6143
pubmed:author
pubmed:issnType
Print
pubmed:volume
293
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C1239-51
pubmed:meshHeading
pubmed-meshheading:17634415-Animals, pubmed-meshheading:17634415-Boron Compounds, pubmed-meshheading:17634415-Caffeine, pubmed-meshheading:17634415-Calcium, pubmed-meshheading:17634415-Calcium Signaling, pubmed-meshheading:17634415-Cells, Cultured, pubmed-meshheading:17634415-Chloride Channels, pubmed-meshheading:17634415-Inositol 1,4,5-Trisphosphate Receptors, pubmed-meshheading:17634415-Kinetics, pubmed-meshheading:17634415-Male, pubmed-meshheading:17634415-Membrane Potentials, pubmed-meshheading:17634415-Myocytes, Smooth Muscle, pubmed-meshheading:17634415-Nifedipine, pubmed-meshheading:17634415-Patch-Clamp Techniques, pubmed-meshheading:17634415-Penis, pubmed-meshheading:17634415-Potassium, pubmed-meshheading:17634415-Rats, pubmed-meshheading:17634415-Rats, Sprague-Dawley, pubmed-meshheading:17634415-Ryanodine, pubmed-meshheading:17634415-Ryanodine Receptor Calcium Release Channel, pubmed-meshheading:17634415-Time Factors
pubmed:year
2007
pubmed:articleTitle
Calcium sparks activate calcium-dependent Cl- current in rat corpus cavernosum smooth muscle cells.
pubmed:affiliation
Department of Physiology and Pharmacology, Schulich School of Medicine & Dentistry, The University of Western Ontario, London, Ontario, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't