The Effect of ۸-Week Aerobic Training on TRPC۶, PMCA۴b levels and Pathological Cardiac Hypertrophy in Middle-Aged Wistar Rats

Cardiac aging is often accompanied by adverse structural and functional changes such as increased left ventricular wall thickness (hypertrophy) and compromised ventricular contractility, termed pathological cardiac hypertrophy. One of the factors affecting pathological cardiac hypertrophy is the amount of intracellular calcium. The Transient receptor potential canonical ۶ (TRPC۶) is a Ca۲+-permeable cation channel presenting in the plasma membrane of many tissues, including the heart tissue. Unlike TRPC۶, plasma membrane Ca۲+ ATPase (PMCA) is a transporter protein in the cellular plasma membrane that maintains an appropriate cytoplasmic Ca۲+ level via removing Ca۲+ from the cell. This study aimed to investigate the effect of moderate aerobic exercise on TRPC۶ and PMCA۴b and dimensions of the heart in the middle-age Wistar rats.Forty Wistar rats including young (n=۱۰, ۴-month-old) and middle-aged rats (n=۳۰, ۱۳-۱۵ months old) were included in this experimental study. All young and ۱۰ middle-aged rats did not exercise and served as a control comparision; while the remaining ۲۰ middle-aged rats were trained at moderate intensity for ۴ week (n=۱۰) or ۸ week (n=۱۰) on a treadmill.PMCA۴b and Left ventricular internal diameter (LVID) were significantly decreased (P=۰.۰۰۱) while TRPC۶ and Left ventricle wall thickness (LVWT) levels were remarkably increased (P=۰.۰۰۱) in the heart tissue of middle-aged compared to the young rats. Aerobic training significantly decreased TRPC۶ (P=۰.۰۰۱) in the middle-aged-T۴ and T۸ groups (P=۰.۰۰۱) compared to the control non- middle-aged rats. However, aerobic training had no effect on PMCA۴b protein expression of in the middle-aged-T۴ and T۸ groups compared middle-aged control groups. LVID was significantly increased in eight weeks, and LVWT was significantly reduced in the eighth week (P=۰.۰۱۱ and P=۰.۰۲۸ respectively).Aerobic training attenuates middle-aged induced pathological cardiac hypertrophy by attenuating TRPC۶.

کلیدواژه ها:

TRCP۶ ، PMCA۴b ، Pathological cardiac hypertrophy