ArticleThe Journal of physiology2007
Signalling mechanisms in contraction-mediated stimulation of intracellular NO production in cat ventricular myocytes.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Akt phosphorylation of neuronal nitric oxide synthase regulates gastrointestinal motility in mouse ileum.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Endogenous nitric oxide formation in cardiac myocytes does not control respiration during β-adrenergic stimulation.The Journal of physiology · 2017Article
- Dystrophin-glycoprotein complex regulates muscle nitric oxide production through mechanoregulation of AMPK signaling.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- S-Nitrosylation of Sarcomeric Proteins Depresses Myofilament Ca2+)Sensitivity in Intact Cardiomyocytes.Antioxidants & redox signaling · 2015Article
- Nanomechanics of vascular endothelium.Cell and tissue research · 2014Review
- Ischemia/Reperfusion injury protection by mesenchymal stem cell derived antioxidant capacity.Stem cells and development · 2013Article
- Nitric oxide regulates cardiac intracellular Na⁺ and Ca²⁺ by modulating Na/K ATPase via PKCε and phospholemman-dependent mechanism.Journal of molecular and cellular cardiology · 2013Article
- Regulation of the cardiac sodium pump.Cellular and molecular life sciences : CMLS · 2013Review
- Contractile Activity Regulates Inducible Nitric Oxide Synthase Expression and NO(i) Production in Cardiomyocytes via a FAK-Dependent Signaling Pathway.Journal of signal transduction · 2012Article
- Myocardial AKT: the omnipresent nexus.Physiological reviews · 2011Review
- Coagulation profiling of random-source cats.Journal of the American Association for Laboratory Animal Science : JAALAS · 2010Article
- Characteristics and function of cardiac mitochondrial nitric oxide synthase.The Journal of physiology · 2009Article
- Laminin acts via focal adhesion kinase/phosphatidylinositol-3' kinase/protein kinase B to down-regulate beta1-adrenergic receptor signalling in cat atrial myocytes.The Journal of physiology · 2009Article
- Impaired acetylcholine-induced smooth muscle contraction in colitis involves altered calcium mobilization and AKT phosphorylation.Pflugers Archiv : European journal of physiology · 2008Article
- Deficient ryanodine receptor S-nitrosylation increases sarcoplasmic reticulum calcium leak and arrhythmogenesis in cardiomyocytes.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In this study we sought to determine whether contractile activity has a role as a signalling mechanism in the activation of intracellular nitric oxide (NO(i)) production induced by electrical stimulation of cat ventricular myocytes. Field stimulation (FS) of single ventricular myocytes elicited frequency-dependent increases in NO(i) that were blocked by the calmodulin (CaM) inhibitor 10 microM W-7 and partially inhibited by the phosphatidylinositol 3'-kinase (PI-(3)K) inhibitor 10 microMm LY294002. Increasing extracellular [Ca(2+)] caused a concentration-dependent increase in FS-induced NO(i) that was partially inhibited by LY294002. The negative inotropic agents BDM (5 mm) or blebbistatin (10 microM) decreased cell shortening and NO(i) production without concomitant changes in L-type Ca(2+) current (I(Ca,L)) or [Ca(2+)](i) transients. The positive inotropic agents EMD 57033 or CGP 48506 (1 microM) increased cell shortening and NO(i) production without concomitant changes in I(Ca,L) or [Ca(2+)](i) transients. FS-induced NO(i) production was decreased in myocytes infected (100 multiplicity of viral infection (MOI); 24 h) with a replication-deficient adenovirus expressing a dominant-negative mutant of protein kinase B (Akt) compared with cells infected with a control adenovirus expressing beta-galactosidase. FS-induced NO(i) was partially inhibited by either endothelial (eNOS) or neuronal nitric oxide synthase (nNOS) inhibitors and completely blocked by simultaneous exposure to both. FS-induced [Ca(2+)](i) transients were increased by the nNOS inhibitor nNOS-I (0.24 microM), decreased by the eNOS inhibitor L-NIO (1 microM) and unchanged by exposure to both inhibitors. We conclude that in cat ventricular myocytes, FS-induced NO(i) production requires both Ca(2+)-dependent CaM signalling and Ca(2+)-independent PI-(3)K-Akt signalling activated by contractile activity. FS activates NO(i) production from both eNOS and nNOS, and each source of NO(i) exerts opposing effects on [Ca(2+)](i) transient amplitude. These findings are important for understanding the regulation of NO(i) signalling in the normal and mechanically failing heart.
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