ArticleThe Journal of clinical investigation1995
Nitric oxide regulates the calcium current in isolated human atrial myocytes.
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed, 195 citations in OpenAlex.
- Compartmentalized cAMP signalling and control of cardiac rhythm.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Mechanisms of cAMP compartmentation in cardiac myocytes: experimental and computational approaches to understanding.The Journal of physiology · 2021Review
- Mind the gap (junction): cGMP induced by nitric oxide in cardiac myocytes originates from cardiac fibroblasts.British journal of pharmacology · 2019Article
- Reducing reperfusion injury during percutaneous coronary intervention.Singapore medical journal · 2019Article
- Metabolic Inhibition Induces Transient Increase of L-type CaInternational journal of molecular sciences · 2019Article
- Reduced density and altered regulation of rat atrial L-type CaAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Perspectives and challenges of antioxidant therapy for atrial fibrillation.Naunyn-Schmiedeberg's archives of pharmacology · 2017Review
- Differences in the control of basal L-type Ca(2+) current by the cyclic AMP signaling cascade in frog, rat, and human cardiac myocytes.The journal of physiological sciences : JPS · 2016Article
- Urocortin 2 stimulates nitric oxide production in ventricular myocytes via Akt- and PKA-mediated phosphorylation of eNOS at serine 1177.American journal of physiology. Heart and circulatory physiology · 2014Article
- β₃-Adrenergic regulation of L-type Ca²⁺ current and force of contraction in human ventricle.The Journal of membrane biology · 2014Article
- Attenuated response of L-type calcium current to nitric oxide in atrial fibrillation.Cardiovascular research · 2014Article
- Study of the regulation of the inotropic response to 5-HT4 receptor activation via phosphodiesterases and its cross-talk with C-type natriuretic peptide in porcine left atrium.Naunyn-Schmiedeberg's archives of pharmacology · 2012Article
- Distinct patterns of constitutive phosphodiesterase activity in mouse sinoatrial node and atrial myocardium.PloS one · 2012Article
- Nitric oxide synthases and atrial fibrillation.Frontiers in physiology · 2012Article
- Agents increasing cyclic GMP amplify 5-HT4-elicited positive inotropic response in failing rat cardiac ventricle.Naunyn-Schmiedeberg's archives of pharmacology · 2011Article
- Atrial natriuretic peptide regulates Ca channel in early developmental cardiomyocytes.PloS one · 2010Article
- Reduced regional myocardial perfusion reserve is associated with impaired contractile performance in idiopathic dilated cardiomyopathy.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2009Article
- Pivotal effects of phosphodiesterase inhibitors on myocyte contractility and viability in normal and ischemic hearts.Acta pharmacologica Sinica · 2009Review
- beta3-adrenergic receptor activation increases human atrial tissue contractility and stimulates the L-type Ca2+ current.The Journal of clinical investigation · 2008Article
- ABCD of the phosphodiesterase family: interaction and differential activity in COPD.International journal of chronic obstructive pulmonary disease · 2008Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac Ca2+ current (ICa) was shown to be regulated by cGMP in a number of different species. Recently, we found that the NO-donor SIN-1 (3-morpholino-sydnonimine) exerts a dual regulation of ICa in frog ventricular myocytes via an accumulation of cGMP. To examine whether NO also regulates Ca2+ channels in human heart, we investigated the effects of SIN-1 on ICa in isolated human atrial myocytes. An extracellular application of SIN-1 produced a profound stimulatory effect on basal ICa at concentrations > 1 pM. Indeed, 10 pM SIN-1 induced a approximately 35% increase in ICa. The stimulatory effect of SIN-1 was maximal at 1 nM (approximately 2-fold increase in ICa) and was comparable with the effect of a saturating concentration (1 microM) of isoprenaline, a beta-adrenergic agonist. Increasing the concentration of SIN-1 to 1-100 microM reduced the stimulatory effect in two thirds of the cells. The stimulatory effect of SIN-1 was not mimicked by SIN-1C, the cleavage product of SIN-1 produced after liberation of NO. This suggests that NO mediates the effects of SIN-1 on ICa. Because, in frog heart, the stimulatory effect of SIN-1 on ICa was found to be due to cGMP-induced inhibition of cGMP-inhibited phosphodiesterase (cGI-PDE), we compared the effects of SIN-1 and milrinone, a cGI-PDE selective inhibitor, on ICa in human. Milrinone (10 microM) induced a strong stimulation of ICa (approximately 150%), demonstrating that cGI-PDE controls the amplitude of basal ICa in this tissue. In the presence of milrinone, SIN-1 (0.1-1 nM) had no stimulatory effect on ICa, suggesting that the effects of SIN-1 and MIL were not additive. We conclude that NO may stimulate ICa in human atrial myocytes via inhibition of the cGI-PDE.
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