ArticleThe Journal of physiology2000
Voltage-dependent Ca2+ release from the SR of feline ventricular myocytes is explained by Ca2+-induced Ca2+ release.
Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 41 citations in OpenAlex.
- Caveolae-localized L-type Ca2+ channels do not contribute to function or hypertrophic signalling in the mouse heart.Cardiovascular research · 2017Article
- Role of RyR2 phosphorylation in heart failure and arrhythmias: protein kinase A-mediated hyperphosphorylation of the ryanodine receptor at serine 2808 does not alter cardiac contractility or cause heart failure and arrhythmias.Circulation research · 2014Review
- Ca2+ influx through T- and L-type Ca2+ channels have different effects on myocyte contractility and induce unique cardiac phenotypes.Circulation research · 2008Article
- Negative inotropic effects of high-mobility group box 1 protein in isolated contracting cardiac myocytes.American journal of physiology. Heart and circulatory physiology · 2008Article
- The inotropic effect of cardioactive glycosides in ventricular myocytes requires Na+-Ca2+ exchanger function.The Journal of physiology · 2006Article
- Synergistic interactions between Ca2+ entries through L-type Ca2+ channels and Na+-Ca2+ exchanger in normal and failing rat heart.The Journal of physiology · 2005Article
- The recombinant dihydropyridine receptor II-III loop and partly structured 'C' region peptides modify cardiac ryanodine receptor activity.The Biochemical journal · 2005Article
- Halothane alters contractility and Ca2+ transport in ventricular myocytes from streptozotocin-induced diabetic rats.Molecular and cellular biochemistry · 2004Article
- Protein phosphatase 1 and an opposing protein kinase regulate steady-state L-type Ca2+ current in mouse cardiac myocytes.The Journal of physiology · 2004Article
- The voltage-sensitive release mechanism of excitation contraction coupling in rabbit cardiac muscle is explained by calcium-induced calcium release.The Journal of general physiology · 2003Article
- Excitation contraction coupling in cardiac muscle: is there a purely voltage-dependent component?The Journal of general physiology · 2003Article
- Heart failure -- a challenge to our current concepts of excitation-contraction coupling.The Journal of physiology · 2003Review
- Regulation of cardiac excitation-contraction coupling by action potential repolarization: role of the transient outward potassium current (I(to)).The Journal of physiology · 2003Review
- A cardiac dihydropyridine receptor II-III loop peptide inhibits resting Ca(2+) sparks in ferret ventricular myocytes.The Journal of physiology · 2001Article
- Modulation of the Ca(2+)-induced Ca(2+) release cascade by beta-adrenergic stimulation in rat ventricular myocytes.The Journal of physiology · 2001Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
1. Direct voltage-gated (voltage-dependent Ca2+ release, VDCR) and Ca2+ influx-gated (Ca2+-induced Ca2+ release, CICR) sarcoplasmic reticulum (SR) Ca2+ release were studied in feline ventricular myocytes. The voltage-contraction relationship predicted by the VDCR hypothesis is sigmoidal with large contractions at potentials near the Ca2+ equilibrium potential (ECa). The relationship predicted by the CICR hypothesis is bell-shaped with no contraction at ECa. 2. The voltage dependence of contraction was measured in ventricular myocytes at physiological temperature (37 C), resting membrane potential and physiological [K+]. Experiments were performed with cyclic adenosine 3',5'-monophosphate (cAMP) in the pipette or in the presence of the beta-adrenergic agonist isoproterenol (isoprenaline; ISO). 3. The voltage-contraction relationship was bell-shaped in Na+-free solutions (to eliminate the Na+ current and Na+-Ca2+ exchange, NCX) but the relationship was broader than the L-type Ca2+ current (ICa,L)-voltage relationship. 4. Contractions induced with voltage steps from normal resting potentials to -40 mV are thought to represent VDCR rather than CICR. We found that cAMP and ISO shifted the voltage dependence of ICa,L activation to more negative potentials so that ICa,L was always present with steps to -40 mV. ICa,L at -40 mV inactivated when the holding potential was decreased (VŁ = -57.8 +/- 0.49 mV). 5. ISO increased inward current, SR Ca2+ load and contraction in physiological [Na+] and a broad bell-shaped voltage-contraction relationship was observed. Inhibition of reverse-mode NCX, decreasing ICa,L and decreasing SR Ca2+ loading all decreased contractions at strongly positive potentials near ECa. 6. The voltage-contraction relationship in 200 microM cadmium (Cd2+) was bell-shaped, supporting a role of ICa,L rather than VDCR. 7. All results could be accounted for by the CICR hypothesis, and many results exclude the VDCR hypothesis.
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