Exercise intensities modulate ACE2/MasR/eNOS pathway in male Wistar rat's lung

Abstract

AbstractSpecific exercise intensities could improve lung vascular function by increasing nitric oxide (NO). The ACE2/MasR/eNOS axis is one of the pathways facilitating NO synthesis. This study examines the effect of different intensities of aerobic training on the ACE2/MasR/eNOS axis and histology of lung muscular arteries. Male Wistar rats were used in this study and randomized into control and exercise groups receiving low‐, moderate‐, and high‐intensity training. The training was conducted for 30 min daily, five times a week, for 8 weeks. We observed that different exercise intensities affect the ACE2/MasR/eNOS pathway differently. Compared to control, high‐intensity aerobic exercise significantly increased ACE2, Mas receptor (MasR), and eNOS mRNA expressions (p < 0.01). Moderate‐intensity exercise significantly increased MasR and eNOS mRNA expressions compared to the control (p < 0.05), and this intensity also increased ACE2 mRNA but not significantly. Low‐intensity exercise increased ACE2, MasR, and eNOS mRNA expressions but not significantly. Low‐, moderate‐, or high‐intensity exercises reduced the medial wall thickness of the lung muscular arteries but not significantly. In conclusion, high‐intensity exercise may induce NO synthesis in the lung by increasing mRNA expression of ACE2, MasR, and eNOS without decreasing the medial wall thickness of the muscular artery. Thus, high‐intensity exercise may be the optimal intensity to improve NO synthesis and vascular function in the lung.