ArticlePflugers Archiv : European journal of physiology2012
Zinc modulation of basal and β-adrenergically stimulated L-type Ca2+ current in rat ventricular cardiomyocytes: consequences in cardiac diseases.
Article in Pflugers Archiv : European journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Importance of Zinc Homeostasis for Normal Cardiac Rhythm.Current cardiology reviews · 2025Review
- Association of serum zinc with mineral stress in chronic kidney disease.Clinical kidney journal · 2024Article
- Exogeneous metal ions as therapeutic agents in cardiovascular disease and their delivery strategies.Regenerative biomaterials · 2024Review
- The role of Zn2+ in shaping intracellular Ca2+ dynamics in the heart.The Journal of general physiology · 2023Review
- The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- Zinc drives vasorelaxation by acting in sensory nerves, endothelium and smooth muscle.Nature communications · 2021Article
- The role of labile ZnMolecular and cellular biochemistry · 2021Review
- The citrus flavanone hesperetin preferentially inhibits slow-inactivating currents of a long QT syndrome type 3 syndrome NaBritish journal of pharmacology · 2019Article
- Sevoflurane Alleviates Reperfusion Arrhythmia by Ameliorating TDR and MAPDAnesthesiology research and practice · 2019Article
- Impact of Labile Zinc on Heart Function: From Physiology to Pathophysiology.International journal of molecular sciences · 2017Review
- The Critical Roles of Zinc: Beyond Impact on Myocardial Signaling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015Review
- The direct modulatory activity of zinc toward ion channels.Integrative medicine research · 2015Review
- Intracellular Zinc Modulates Cardiac Ryanodine Receptor-mediated Calcium Release.The Journal of biological chemistry · 2015Article
- Cinnamaldehyde inhibits L-type calcium channels in mouse ventricular cardiomyocytes and vascular smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014Article
- Zinc and the prooxidant heart failure phenotype.Journal of cardiovascular pharmacology · 2014Review
- Sex-dependent, zinc-induced dephosphorylation of phospholamban by tissue-nonspecific alkaline phosphatase in the cardiac sarcomere.American journal of physiology. Heart and circulatory physiology · 2014Article
- Differential metal content and gene expression in rat left ventricular hypertrophy due to hypertension and hyperactivity.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2014Article
- Contribution of calcium-conducting channels to the transport of zinc ions.Pflugers Archiv : European journal of physiology · 2014Review
- Extracellular zinc ion regulates transient receptor potential melastatin 5 (TRPM5) channel activation through its interaction with a pore loop domain.The Journal of biological chemistry · 2013Article
- ß-blocker timolol prevents arrhythmogenic Ca²⁺ release and normalizes Ca²⁺ and Zn²⁺ dyshomeostasis in hyperglycemic rat heart.PloS one · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zinc exists in biological systems as bound and histochemically reactive free Zn(2+) in the nanomolar range. Zinc is required as either structural or catalytic component for a large number of enzymes. It also modulates current passage through many ion channels. Here, we reinvestigated the effects of extracellular and intracellular Zn(2+) on the L-type Ca(2+) current (I (CaL)) and its modulation by β-adrenergic stimulation in rat ventricular cardiomyocytes. In the absence of Ca(2+) ions, Zn(2+) could permeate through the L-type channel at much lower concentrations and at a more positive voltage range, but with a lower permeability than Ca(2+). In the presence of Ca(2+), extracellular Zn(2+) demonstrated strong bimodal inhibitory effects on the I (CaL), with half-inhibition occurring around 30 nM, i.e., in the range of concentrations found in the plasma. Intracellular Zn(2+) also significantly inhibited the I (CaL) with a half-inhibitory effect at 12.7 nM. Moreover, β-adrenergic stimulation was markedly reduced by intracellular Zn(2+) at even lower concentrations (<1 nM) as a consequence of Zn(2+)-induced inhibition of the adenylyl cyclase. All these effects appeared independent of redox variations and were not affected by dithiothreitol. Thus, both basal intracellular and extracellular Zn(2+) modulate transmembrane Ca(2+) movements and their regulation by β-adrenergic stimulation. Considering that, in many pathological situations, including diabetes, the extracellular Zn(2+) concentration is reduced and the intracellular one is increased, our results help to explain both Ca(2+) overload and marked reduction in the β-adrenergic stimulation in these diseases.
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