ArticleThe Journal of physiology1995
A sustained inward current activated at the diastolic potential range in rabbit sino-atrial node cells.
Article in The Journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 132 citations in OpenAlex.
- Gradient-based parameter optimization method to determine membrane ionic current composition in human induced pluripotent stem cell-derived cardiomyocytes.Scientific reports · 2022Trial
- Pacemaker Channels and the Chronotropic Response in Health and Disease.Circulation research · 2024Review
- Reciprocal interaction between IK1 and If in biological pacemakers: A simulation study.PLoS computational biology · 2021Article
- Pacemaking in cardiac tissue. From IK2 to a coupled-clock system.Physiological reports · 2019Review
- Unique CaInternational journal of molecular sciences · 2018Review
- Heterogeneous functional expression of the sustained inward NaPflugers Archiv : European journal of physiology · 2018Article
- CaScientific reports · 2017Article
- Mechanisms underlying the cardiac pacemaker: the role of SK4 calcium-activated potassium channels.Acta pharmacologica Sinica · 2016Review
- Modern perspectives on numerical modeling of cardiac pacemaker cell.Journal of pharmacological sciences · 2014Review
- Contribution of quantitative changes in individual ionic current systems to the embryonic development of ventricular myocytes: a simulation study.The journal of physiological sciences : JPS · 2013Article
- Numerical models based on a minimal set of sarcolemmal electrogenic proteins and an intracellular Ca(2+) clock generate robust, flexible, and energy-efficient cardiac pacemaking.Journal of molecular and cellular cardiology · 2013Article
- NALCN: a regulator of pacemaker activity.Molecular neurobiology · 2012Review
- Modeling the chronotropic effect of isoprenaline on rabbit sinoatrial node.Frontiers in physiology · 2012Article
- A mathematical model of action potentials of mouse sinoatrial node cells with molecular bases.American journal of physiology. Heart and circulatory physiology · 2011Article
- A coupled SYSTEM of intracellular Ca2+ clocks and surface membrane voltage clocks controls the timekeeping mechanism of the heart's pacemaker.Circulation research · 2010Review
- Effects of muscarinic receptor stimulation on Ca2+ transient, cAMP production and pacemaker frequency of rabbit sinoatrial node cells.Basic research in cardiology · 2010Article
- The Contribution of HCN4 to normal sinus node function in humans and animal models.Pacing and clinical electrophysiology : PACE · 2010Review
- Regulation of basal and reserve cardiac pacemaker function by interactions of cAMP-mediated PKA-dependent Ca2+ cycling with surface membrane channels.Journal of molecular and cellular cardiology · 2009Review
- The missing link in the mystery of normal automaticity of cardiac pacemaker cells.Annals of the New York Academy of Sciences · 2008Review
- Cardiac pacemaker function of HCN4 channels in mice is confined to embryonic development and requires cyclic AMP.The EMBO journal · 2008Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. After blocking both the hyperpolarization-activated current and the membrane K+ conductance, depolarizations from -80 mV to between -70 and -50 mV induced a sustained current in sino-atrial node cells. We have tentatively designated this current Ist. 2. Ist was blocked by both organic and inorganic Ca2+ channel blockers, but was insensitive to tetrodotoxin (30 microM). Isoprenaline increased Ist. 3. The peak of Ist (at about -50 mV) was increased to 149 +/- 13% (n = 8, P < 0.01) by lowering the external Ca2+ concentration ([Ca2+]o) from 1.8 to 0.1 mM, in contrast to the marked depression of the L-type Ca2+ current. In 0.1 mM [Ca2+]o solution, the nicardipine-sensitive current-voltage relation showed the peak amplitude at about -50 mV and a reversal potential of +37.4 +/- 4.4 mV (n = 5). The isoprenaline-sensitive component also showed a reversal potential of about +30 mV. 4. Reducing [Na+]o from 140 to 70 mM in 0.1 mM [Ca2+]o decreased Ist to 53 +/- 5% (n = 7, P < 0.01). Increasing [Ca2+]o or [Mg2+]o decreased the amplitude of Ist. The half-maximum concentration of Mg2+ inhibition was 2.2 mM. 5. At 1.8 mM [Ca2+]o, Ist was inactivated by clamping for 5s at -10 mV, and gradually recovered after repolarization to -80 mV with a half-time of 1.36 +/- 0.4 s (n = 6). 6. The transitional sino-atrial node cell had minimal amplitude of Ist. 7. These characteristics of Ist are qualitatively comparable to those of the monovalent cation conductance of the L-type Ca2+ channel induced by depleting external divalent cations to the micromolar range. We conclude that Ist is generated by a novel subtype of L-type Ca2+ channel.
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