ArticleAmerican journal of physiology. Heart and circulatory physiology2007
Ca(v)1.3 channels produce persistent calcium sparklets, but Ca(v)1.2 channels are responsible for sparklets in mouse arterial smooth muscle.
Article in American journal of physiology. Heart and circulatory physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed, 59 citations in OpenAlex.
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- Ion channels expression and function are strongly modified in solid tumors and vascular malformations.Journal of translational medicine · 2016Article
- Ca(2+) entry into neurons is facilitated by cooperative gating of clustered CaV1.3 channels.eLife · 2016Article
- Membrane potential and Ca2+ concentration dependence on pressure and vasoactive agents in arterial smooth muscle: A model.The Journal of general physiology · 2015Article
- Article
- Calcineurin/nuclear factor of activated T cells-coupled vanilliod transient receptor potential channel 4 ca2+ sparklets stimulate airway smooth muscle cell proliferation.American journal of respiratory cell and molecular biology · 2014Article
- L-type Ca2+ channel sparklets revealed by TIRF microscopy in mouse urinary bladder smooth muscle.PloS one · 2014Article
- Caveolin-1 facilitates the direct coupling between large conductance Ca2+-activated K+ (BKCa) and Cav1.2 Ca2+ channels and their clustering to regulate membrane excitability in vascular myocytes.The Journal of biological chemistry · 2013Article
- Regulation of L-type calcium channel sparklet activity by c-Src and PKC-α.American journal of physiology. Cell physiology · 2013Article
- Harmonin enhances voltage-dependent facilitation of Cav1.3 channels and synchronous exocytosis in mouse inner hair cells.The Journal of physiology · 2013Article
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7 authors at 2 institutions in 2 countries.
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Abstract
Ca(2+) sparklets are local elevations in intracellular Ca(2+) produced by the opening of a single or a cluster of L-type Ca(2+) channels. In arterial myocytes, Ca(2+) sparklets regulate local and global intracellular Ca(2+). At present, the molecular identity of the L-type Ca(2+) channels underlying Ca(2+) sparklets in these cells is undetermined. Here, we tested the hypotheses that voltage-gated calcium channel-alpha 1.3 subunit (Ca(v)1.3) can produce Ca(2+) sparklets and that Ca(v)1.2 and/or Ca(v)1.3 channels are responsible for Ca(2+) sparklets in mouse arterial myocytes. First, we investigated the functional properties of single Ca(v)1.3 channels in tsA201 cells. With 110 mM Ba(2+) as the charge carrier, Ca(v)1.3 channels had a conductance of 20 pS. This value is similar to that of Ca(v)1.2 and native L-type Ca(2+) channels. As previously shown for Ca(v)1.2 channels, Ca(v)1.3 channels can operate in two gating modes characterized by short and long open times. Expressed Ca(v)1.3 channels also produced Ca(2+) sparklets. Ca(v)1.3 sparklets had properties similar to those produced by Ca(v)1.2 and native L-type channels, including quantal amplitude, dihydropyridine sensitivity, bimodal gating, and dual-event duration times. However, the voltage dependencies of conductance and steady-state inactivation of the Ca(2+) current (I(Ca)) in arterial myocytes were similar to those recorded from cells expressing Ca(v)1.2 but not Ca(v)1.3 channels. Furthermore, nifedipine (10 microM) eliminated Ca(2+) sparklets in wild-type myocytes but not in myocytes expressing dihydropyridine-insensitive Ca(v)1.2 channels. Accordingly, Ca(v)1.3 transcript and protein were not detected in isolated arterial myocytes. We conclude that although Ca(v)1.3 channels can produce Ca(2+) sparklets, Ca(v)1.2 channels underlie I(Ca), Ca(2+) sparklets, and hence dihydropyridine-sensitive Ca(2+) influx in mouse arterial myocytes.
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