ArticleThe Journal of physiology2005
Phenylephrine acts via IP3-dependent intracellular NO release to stimulate L-type Ca2+ current in cat atrial myocytes.
Article in The Journal of physiology, 2005. 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, 35 citations in OpenAlex.
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- In Vivo Antihypertensive and Ex Vivo Vasodilatory Studies of Taxifolin.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Mechanisms of stretch-induced electro-anatomical remodeling and atrial arrhythmogenesis.Journal of molecular and cellular cardiology · 2024Review
- Timing mechanisms to control heart rhythm and initiate arrhythmias: roles for intracellular organelles, signalling pathways and subsarcolemmal CaPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Adrenoceptor sub-type involvement in CaPflugers Archiv : European journal of physiology · 2022Article
- Inositol 1,4,5-trisphosphate receptors in cardiomyocyte physiology and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Inhibition of adenylyl cyclase 1 by ST034307 inhibits IPFrontiers in pharmacology · 2022Article
- IPAmerican journal of physiology. Heart and circulatory physiology · 2021Article
- Mechanisms Underlying Spontaneous Action Potential Generation Induced by Catecholamine in Pulmonary Vein Cardiomyocytes: A Simulation Study.International journal of molecular sciences · 2019Article
- Article
- Microdomain-specific localization of functional ion channels in cardiomyocytes: an emerging concept of local regulation and remodelling.Biophysical reviews · 2015Article
- Mechanisms by which calcium receptor stimulation modifies electromechanical coupling in isolated ventricular cardiomyocytes.Pflugers Archiv : European journal of physiology · 2015Article
- The flavonoid luteolin induces nitric oxide production and arterial relaxation.European journal of nutrition · 2014Article
- Laminin enhances beta(2)-adrenergic receptor stimulation of L-type Ca(2+) current via cytosolic phospholipase A(2) signalling in cat atrial myocytes.The Journal of physiology · 2009Article
- Characteristics and function of cardiac mitochondrial nitric oxide synthase.The Journal of physiology · 2009Article
- Ginsenoside Re suppresses electromechanical alternans in cat and human cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2008Article
- Signalling mechanisms in contraction-mediated stimulation of intracellular NO production in cat ventricular myocytes.The Journal of physiology · 2007Article
- The MLCK-mediated alpha1-adrenergic inotropic effect in atrial myocardium is negatively modulated by PKCepsilon signaling.British journal of pharmacology · 2006Article
- Modulation by brain natriuretic peptide of GABA receptors on rat retinal ON-type bipolar cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Caveolae, ion channels and cardiac arrhythmias.Progress in biophysics and molecular biologyReview
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
This study determined the effects of alpha1-adrenergic receptor (alpha1-AR) stimulation by phenylephrine (PE) on L-type Ca2+ current (I(Ca,L)) in cat atrial myocytes. PE (10 microm) reversibly increased I(Ca,L) (51.3%; n = 40) and shifted peak I(Ca,L) activation voltage by -10 mV. PE-induced stimulation of I(Ca,L) was blocked by each of 1 microm prazocin, 10 microm L-NIO, 10 microm W-7, 10 microm ODQ, 2 microm H-89 or 10 microm LY294002, and was unaffected by 10 microm chelerythrine or incubating cells in pertussis toxin (PTX). PE-induced stimulation of I(Ca,L) also was inhibited by each of 10 microm ryanodine or 5 microm thapsigargin, by blocking IP3 receptors with 2 microm 2-APB or 10 microm xestospongin C or by intracellular dialysis of heparin. In field-stimulated cells, PE increased intracellular NO (NOi) production. PE-induced NOi release was inhibited by each of 1 microm prazocin, 10 microm L-NIO, 10 microm W-7, 10 microm LY294002, 2 microm H-89, 10 microm ryanodine, 5 microm thapsigargin, 2 microm 2-APB or 10 microm xestospongin C, and unchanged by PTX. PE (10 microm) increased phosphorylation of Akt, which was inhibited by LY294002. Confocal microscopy showed that PE stimulated NOi release from subsarcolemmal sites and this was prevented by 2 mm methyl-beta-cyclodextrin, an agent that disrupts caveolae formation. PE also increased local, subsarcolemmal SR Ca2+ release via IP3-dependent signalling. Electron micrographs of atrial myocytes show peripheral SR cisternae in close proximity to clusters of caveolae. We conclude that in cat atrial myocytes PE acts via alpha1-ARs coupled to PTX-insensitive G-protein to release NOi, which in turn stimulates I(Ca,L). PE-induced NOi release requires stimulation of both PI-3K/Akt and IP3-dependent Ca2+ signalling. NO stimulates I(Ca,L) via cGMP-mediated cAMP-dependent PKA signalling. IP3-dependent Ca2+ signalling may enhance local SR Ca2+ release required to activate Ca2+-dependent eNOS/NOi production from subsarcolemmal caveolae sites.
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