Nitric Oxide and Mechano-Electrical Transduction in Cardiomyocytes

一氧化氮 一氧化氮合酶 NOS1号 信号转导 心力衰竭 调解人 细胞生物学 心房颤动 化学 药理学 医学 内科学 生物
作者
Hannah E Boycott,My-Nhan Nguyen,Besarte Vrellaku,Katja Gehmlich,Paul Robinson
出处
期刊:Frontiers in Physiology [Frontiers Media SA]
卷期号:11 被引量:5
标识
DOI:10.3389/fphys.2020.606740
摘要

The ability § of the heart to adapt to changes in the mechanical environment is critical for normal cardiac physiology. The role of nitric oxide is increasingly recognized as a mediator of mechanical signaling. Produced in the heart by nitric oxide synthases, nitric oxide affects almost all mechano-transduction pathways within the cardiomyocyte, with roles mediating mechano-sensing, mechano-electric feedback (via modulation of ion channel activity), and calcium handling. As more precise experimental techniques for applying mechanical stresses to cells are developed, the role of these forces in cardiomyocyte function can be further understood. Furthermore, specific inhibitors of different nitric oxide synthase isoforms are now available to elucidate the role of these enzymes in mediating mechano-electrical signaling. Understanding of the links between nitric oxide production and mechano-electrical signaling is incomplete, particularly whether mechanically sensitive ion channels are regulated by nitric oxide, and how this affects the cardiac action potential. This is of particular relevance to conditions such as atrial fibrillation and heart failure, in which nitric oxide production is reduced. Dysfunction of the nitric oxide/mechano-electrical signaling pathways are likely to be a feature of cardiac pathology (e.g., atrial fibrillation, cardiomyopathy, and heart failure) and a better understanding of the importance of nitric oxide signaling and its links to mechanical regulation of heart function may advance our understanding of these conditions.
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