ArticleThe Journal of physiology1997
Extracellular divalent cations block a cation non-selective conductance unrelated to calcium channels in rat cardiac muscle.
Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 65 citations in OpenAlex.
- Article
- Modulation of Human Cardiac TRPM7 Current by Extracellular Acidic pH Depends upon Extracellular Concentrations of Divalent Cations.PloS one · 2017Article
- Characterization of Mg²⁺-regulated TRPM7-like current in human atrial myocytes.Journal of biomedical science · 2012Article
- Reductions in external divalent cations evoke novel voltage-gated currents in sensory neurons.PloS one · 2012Article
- Induction of a novel cation current in cardiac ventricular myocytes by flufenamic acid and related drugs.British journal of pharmacology · 2010Article
- The Mg2+ and Mg(2+)-nucleotide-regulated channel-kinase TRPM7.Handbook of experimental pharmacology · 2007Review
- Emergence of a spermine-sensitive, non-inactivating conductance in mature hippocampal CA1 pyramidal neurons upon reduction of extracellular Ca2+: dependence on intracellular Mg2+ and ATP.Neurochemistry international · 2007Article
- Magnesium-inhibited, TRPM6/7-like channel in cardiac myocytes: permeation of divalent cations and pH-mediated regulation.The Journal of physiology · 2004Article
- Hypocretin/orexin innervation and excitation of identified septohippocampal cholinergic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Identification of a non-selective cation channel current in myometrial cells isolated from pregnant rats.Pflugers Archiv : European journal of physiology · 2004Article
- Acidosis decreases low Ca(2+)-induced neuronal excitation by inhibiting the activity of calcium-sensing cation channels in cultured mouse hippocampal neurons.The Journal of physiology · 2003Article
- Alpha 1-adrenoceptor-activated cation currents in neurones acutely isolated from rat cardiac parasympathetic ganglia.The Journal of physiology · 2003Article
- Monovalent cation (MC) current in cardiac and smooth muscle cells: regulation by intracellular Mg2+ and inhibition by polycations.British journal of pharmacology · 2003Article
- Calcium-impermeable monovalent cation channels: a TRP connection?British journal of pharmacology · 2003Review
- Distinct properties of CRAC and MIC channels in RBL cells.The Journal of general physiology · 2002Article
- Changes in extracellular Ca2+ can affect the pattern of discharge in rat thalamic neurons.The Journal of physiology · 2001Article
- Membrane currents in cultured human intestinal smooth muscle cells.The Journal of physiology · 2000Article
- Stretch-activated and background non-selective cation channels in rat atrial myocytes.The Journal of physiology · 2000Article
- Contribution of Ca2+-activated K+ channels and non-selective cation channels to membrane potential of pulmonary arterial smooth muscle cells of the rabbit.The Journal of physiology · 1999Article
- Monovalent cation and L-type Ca2+ channels participate in calcium paradox-like phenomenon in rabbit aortic smooth muscle cells.The Journal of physiology · 1999Article
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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. The effect of removing extracellular divalent cations on resting potential (Vrest) and background conductance of rat cardiac muscle was studied. Vrest was measured with 3 M KCl-filled microelectrodes in papillary muscles, or with a patch electrode in ventricular myocytes. Whole-cell membrane currents were measured in myocytes using step or ramp voltage commands. 2. In both muscles and single cells, decrease or removal of Ca2+o and Mg2+o caused a nifedipine-resistant depolarization, which was reversed upon readmission of Ca2+o or Mg2+o (half-maximal effect at 0.8 mM Ca2+o or 3 mM Mg2+o in muscles). 3. In single myocytes, removal of Ca2+o and Mg2+o had no effect on the seal resistance in nonruptured cell-attached recordings, but reversibly induced a current with a reversal potential (Vrev) of -8 +/- 3.4 mV (with internal Cs+; mean +/- S.E.M., n = 23) during whole-cell recordings. The current was insensitive to nifedipine (3-100 microM) or amiloride (1 mM). Vrev was insensitive to changes in the equilibrium potential for chloride ions (ECl). 4. The current induced in the absence of extracellular divalent cations was blocked in a concentration-dependent manner by Ca2+o. (At -80 mV, the affinity constant KCa was 60 microM with a Hill coefficient of 0.9) KCa was voltage dependent at positive but not negative potentials. Mg2+o, Ni2+o, Sr2+o, Ba2+o, Cd2+o and Gd3+o also blocked the current. 5. In 0 mM Na+ (145 mM NMDG+), the inward component of the divalent cation-sensitive current was decreased and Vrev shifted to more negative potentials. 6. These results suggest that a novel conductance pathway, permeable to monovalent cations but not to Cl- and blocked by divalent cations, exists in ventricular myocytes.
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