ArticleThe Journal of physiology2007
C-type natriuretic peptide activates a non-selective cation current in acutely isolated rat cardiac fibroblasts via natriuretic peptide C receptor-mediated signalling.
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 37 papers.
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Who cites it
37 citing papers in PubMed, 79 citations in OpenAlex.
- CaBiomedicines · 2025Review
- Long QT syndrome type 3 gain-of-function of NaCommunications biology · 2025Article
- Transient Receptor Potential Canonical 5 (TRPC5): Regulation of Heart Rate and Protection against Pathological Cardiac Hypertrophy.Biomolecules · 2024Article
- Transcriptomic profile of the mechanosensitive ion channelome in human cardiac fibroblasts.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- C Type Natriuretic Peptide Receptor Activation Inhibits Sodium Channel Activity in Human Aortic Endothelial Cells by Activating the Diacylglycerol-Protein Kinase C Pathway.International journal of molecular sciences · 2022Article
- Monitoring TRPC7 Conformational Changes by BRET Following GPCR Activation.International journal of molecular sciences · 2022Article
- TRPM4 non-selective cation channel in human atrial fibroblast growth.Pflugers Archiv : European journal of physiology · 2020Article
- CaBritish journal of pharmacology · 2020Review
- Angiotensin-II-Evoked CaCells · 2020Article
- TRPC Channels: Dysregulation and CaCells · 2020Review
- Inherited Cardiac Arrhythmia Syndromes: Focus on Molecular Mechanisms Underlying TRPM4 Channelopathies.Cardiovascular therapeutics · 2020Review
- CaJournal of cardiovascular development and disease · 2019Review
- Transient Receptor Potential Canonical 3 and Nuclear Factor of Activated T Cells C3 Signaling Pathway Critically Regulates Myocardial Fibrosis.Antioxidants & redox signaling · 2019Article
- Transient receptor potential channels in cardiac health and disease.Nature reviews. Cardiology · 2019Review
- C-type Natriuretic Peptide: A Multifaceted Paracrine Regulator in the Heart and Vasculature.International journal of molecular sciences · 2019Review
- Natriuretic peptide activation of extracellular regulated kinase 1/2 (ERK1/2) pathway by particulate guanylyl cyclases in GH3 somatolactotropes.Cell and tissue research · 2017Article
- The Soft- and Hard-Heartedness of Cardiac Fibroblasts: Mechanotransduction Signaling Pathways in Fibrosis of the Heart.Journal of clinical medicine · 2017Review
- Fibroblast-myocyte coupling in the heart: Potential relevance for therapeutic interventions.Journal of molecular and cellular cardiology · 2016Review
- A review of the literature on cardiac electrical activity between fibroblasts and myocytes.Progress in biophysics and molecular biology · 2016Review
- Impaired sinoatrial node function and increased susceptibility to atrial fibrillation in mice lacking natriuretic peptide receptor C.The Journal of physiology · 2015Article
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
In the heart, fibroblasts play an essential role in the deposition of the extracellular matrix and they also secrete a number of hormonal factors. Although natriuretic peptides, including C-type natriuretic peptide (CNP) and brain natriuretic peptide, have antifibrotic effects on cardiac fibroblasts, the effects of CNP on fibroblast electrophysiology have not been examined. In this study, acutely isolated ventricular fibroblasts from the adult rat were used to measure the effects of CNP (2 x 10(-8) M) under whole-cell voltage-clamp conditions. CNP, as well as the natriuretic peptide C receptor (NPR-C) agonist cANF (2 x 10(-8) M), significantly increased an outwardly rectifying non-selective cation current (NSCC). This current has a reversal potential near 0 mV. Activation of this NSCC by cANF was abolished by pre-treating fibroblasts with pertussis toxin, indicating the involvement of G(i) proteins. The cANF-activated NSCC was inhibited by the compounds Gd(3+), SKF 96365 and 2-aminoethoxydiphenyl borate. Quantitative RT-PCR analysis of mRNA from rat ventricular fibroblasts revealed the expression of several transient receptor potential (TRP) channel transcripts. Additional electrophysiological analysis showed that U73122, a phospholipase C antagonist, inhibited the cANF-activated NSCC. Furthermore, the effects of CNP and cANF were mimicked by the diacylglycerol analogue 1-oleoyl-2-acetyl-sn-glycerol (OAG), independently of protein kinase C activity. These are defining characteristics of specific TRPC channels. More detailed molecular analysis confirmed the expression of full-length TRPC2, TRPC3 and TRPC5 transcripts. These data indicate that CNP, acting via the NPR-C receptor, activates a NSCC that is at least partially carried by TRPC channels in cardiac fibroblasts.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.