ArticleThe Journal of pharmacology and experimental therapeutics2010
Interaction between sensory C-fibers and cardiac mast cells in ischemia/reperfusion: activation of a local renin-angiotensin system culminating in severe arrhythmic dysfunction.
Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Effect of Danhong injection on prognosis and inflammatory factor expression in patients with acute coronary syndrome during the perioperative period of percutaneous coronary intervention: A systematic review and meta-analysis.Frontiers in cardiovascular medicine · 2022Pooled it
- The neuroimmune axis in cardiovascular disease: from immune activation to inflammatory resolution.Frontiers in immunology · 2026Review
- Cardiovascular manifestations in mast cell activation disease: key insights for cardiologists and angiologists.Frontiers in cardiovascular medicine · 2025Review
- Mast cells: a novel therapeutic avenue for cardiovascular diseases?Cardiovascular research · 2024Review
- Cardiac risk stratification of the liver transplant candidate: A comprehensive review.World journal of transplantation · 2022Review
- Histamine receptors in heart failure.Heart failure reviews · 2022Review
- Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning.International journal of molecular sciences · 2022Review
- Future Needs in Mast Cell Biology.International journal of molecular sciences · 2019Review
- Immune cells as targets for cardioprotection: new players and novel therapeutic opportunities.Cardiovascular research · 2019Review
- Substance P-mediated cardiac mast cell activation: An in vitro study.Neuropeptides · 2019Article
- Ambroxol for the treatment of fibromyalgia: science or fiction?Journal of pain research · 2017Article
- E-NTPDase1/CD39 modulates renin release from heart mast cells during ischemia/reperfusion: a novel cardioprotective role.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- IgE receptor-mediated mast-cell renin release.The American journal of pathology · 2014Article
- Roles of sensory nerves in the regulation of radiation-induced structural and functional changes in the heart.International journal of radiation oncology, biology, physics · 2014Article
- Substance P in heart failure: the good and the bad.International journal of cardiology · 2014Review
- Inotropic and lusitropic effects of calcitonin gene-related peptide in the heart.American journal of physiology. Heart and circulatory physiology · 2013Article
- Article
- Remodeling of intrinsic cardiac neurons: effects of β-adrenergic receptor blockade in guinea pig models of chronic heart disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2012Article
- Aldehyde dehydrogenase type 2 activation by adenosine and histamine inhibits ischemic norepinephrine release in cardiac sympathetic neurons: mediation by protein kinase Cε.The Journal of pharmacology and experimental therapeutics · 2012Article
- Histamine 3 receptor activation reduces the expression of neuronal angiotensin II type 1 receptors in the heart.The Journal of pharmacology and experimental therapeutics · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Renin, the rate-limiting enzyme in the activation of the renin-angiotensin system (RAS), is synthesized and stored in cardiac mast cells. In ischemia/reperfusion, cardiac sensory nerves release neuropeptides such as substance P that, by degranulating mast cells, might promote renin release, thus activating a local RAS and ultimately inducing cardiac dysfunction. We tested this hypothesis in whole hearts ex vivo, in cardiac nerve terminals in vitro, and in cultured mast cells. We found that substance P-containing nerves are juxtaposed to renin-containing cardiac mast cells. Chemical stimulation of these nerves elicited substance P release that was accompanied by renin release, with the latter being preventable by mast cell stabilization or blockade of substance P receptors. Substance P caused degranulation of mast cells in culture and elicited renin release, and both of these were prevented by substance P receptor blockade. Ischemia/reperfusion in ex vivo hearts caused the release of substance P, which was associated with an increase in renin and norepinephrine overflow and with sustained reperfusion arrhythmias; substance P receptor blockade prevented these changes. Substance P, norepinephrine, and renin were also released by acetaldehyde, a known product of ischemia/reperfusion, from cardiac synaptosomes and cultured mast cells, respectively. Collectively, our findings indicate that an important link exists in the heart between sensory nerves and renin-containing mast cells; substance P released from sensory nerves plays a significant role in the release of mast cell renin in ischemia/reperfusion and in the activation of a local cardiac RAS. This culminates in angiotensin production, norepinephrine release, and arrhythmic cardiac dysfunction.
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