Journal Article Research Support, Non-U.S. Gov't Epublish 5 citations
PubMed: 38254656 DOI: 10.3390/biom14010057
Disruption of Atrial Rhythmicity by the Air Pollutant 1,2-Naphthoquinone: Role of Beta-Adrenergic and Sensory Receptors.
Biomolecules 14(1)
Authors: Antonio G Soares, Simone A Teixeira, Pratish Thakore, Larissa G Santos, Walter Dos R P Filho, Vagner R Antunes, Marcelo N Muscará, Susan D Brain, Soraia K P Costa
Affiliations
- Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, Av. Prof Lineu Prestes, 1524, São Paulo 05508-000, SP, Brazil.
- Department of Integrative Biology and Pharmacology, University of Texas Health Science Center at Houston, 6431 Fannin St. Houston, TX 77030, USA.
- Section of Vascular Biology and Inflammation, School of Cardiovascular Medicine and Sciences, BHF Cardiovascular Centre of Research Excellence, King's College London, Franklin-Wilkins Building, London SE1 9NH, UK.
- Fundação Jorge Duprat Figueiredo de Segurança e Medicina do Trabalho, Ministério do Trabalho e Previdência Social, Rua Capote Valente, nº 710, São Paulo 05409-002, SP, Brazil.
- Departamento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas, Universidade de São Paulo, Av. Prof Lineu Prestes, 1524, São Paulo 05508-000, SP, Brazil.
Abstract
The combustion of fossil fuels contributes to air pollution (AP), which was linked to about 8.79 million global deaths in 2018, mainly due to respiratory and cardiovascular-related effects. Among these, particulate air pollution (PM2.5) stands out as a major risk factor for heart health, especially during vulnerable phases. Our prior study showed that premature exposure to 1,2-naphthoquinone (1,2-NQ), a chemical found in diesel exhaust particles (DEP), exacerbated asthma in adulthood. Moreover, increased concentration of 1,2-NQ contributed to airway inflammation triggered by PM2.5, employing neurogenic pathways related to the up-regulation of transient receptor potential vanilloid 1 (TRPV1). However, the potential impact of early-life exposure to 1,2-naphthoquinone (1,2-NQ) on atrial fibrillation (AF) has not yet been investigated. This study aims to investigate how inhaling 1,2-NQ in early life affects the autonomic adrenergic system and the role played by TRPV1 in these heart disturbances. C57Bl/6 neonate male mice were exposed to 1,2-NQ (100 nM) or its vehicle at 6, 8, and 10 days of life. Early exposure to 1,2-NQ impairs adrenergic responses in the right atria without markedly affecting cholinergic responses. ECG analysis revealed altered rhythmicity in young mice, suggesting increased sympathetic nervous system activity. Furthermore, 1,2-NQ affected β1-adrenergic receptor agonist-mediated positive chronotropism, which was prevented by metoprolol, a β1 receptor blocker. Capsazepine, a TRPV1 blocker but not a TRPC5 blocker, reversed 1,2-NQ-induced cardiac changes. In conclusion, neonate mice exposure to AP 1,2-NQ results in an elevated risk of developing cardiac adrenergic dysfunction, potentially leading to atrial arrhythmia at a young age.
MeSH
Adrenergic Agents, Infant, Newborn, Environmental Pollutants, Air Pollution, Heart Failure, Heart, Atrial Fibrillation, Air, Receptors, Adrenergic, Naphthoquinones, Environmental Pollution, Air Pollutants, Periodicity, Sensory Receptor Cells, Particulate Matter