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Discrete Stretch Eliminates Electrophysiological Dose-Dependent Effects of Nitric Oxide Donor SNAP in Rat Atrium
A L Shim1, V M Mitrokhin2, V E Kazanski1
1Department of Physiology, N. I. Pirogov Russian National Research Medical University, Ministry of Health of the Russian Federation, Moscow, Russia.
Abstract:
Depolarization of cardiomyocytes triggered by stretch and activation of mechanically gated ion channels can lead to serious arrhythmias. However, stretch-induced signaling activating these channels remain little studied. This study tested the hypothesis on implication of NO in shaping the electrical abnormalities provoked by stretch of the right atrial myocardium in rat via a mechanism engaging a signaling cascade, where NO plays a significant role. This approach showed that in isolated right atrial preparation, NO donor SNAP induces the electrical abnormalities similar to those provoked by stretch, and the latter results from activation of NO synthase.
Insights
Stretch-induced arrhythmias involve mechanically gated ion channels. This study reveals nitric oxide (NO) activates NO synthase, leading to electrical abnormalities in atrial myocardium, similar to stretch effects.
Area of Science:
- Cardiovascular Physiology
- Cardiac Electrophysiology
- Molecular Signaling
Background:
- Stretch-activated ion channels in cardiomyocytes can cause arrhythmias.
- Stretch-induced signaling pathways activating these channels are not well understood.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in stretch-induced electrical abnormalities in rat right atrial myocardium.
- To test the hypothesis that NO is involved in a signaling cascade triggered by myocardial stretch.
Main Methods:
- Isolated right atrial preparations from rats were used.
- Electrical abnormalities induced by stretch were recorded.
- The effect of NO donor SNAP and NO synthase activation were examined.
Main Results:
- Nitric oxide (NO) donor SNAP mimicked the electrical abnormalities caused by stretch.
- Stretch-induced electrical abnormalities resulted from the activation of NO synthase.
- This suggests a signaling cascade involving NO in response to stretch.
Conclusions:
- Nitric oxide plays a significant role in the electrical abnormalities of the right atrial myocardium provoked by stretch.
- Activation of NO synthase is a key mechanism linking stretch to these electrical changes.
- Further research into NO-mediated signaling could offer new therapeutic targets for arrhythmias.
