ABSTRACT
To explore the role of mechanosensitive potassium channel TREK-1, Western blot analysis was used to investigate the expression changes of TREK-1 in left ventricle in acute mechanically stretched heart. Forty Wistar rats were randomly divided into 8 groups (n=5 in each group), subject to single Langendorff perfusion for 0, 30, 60, 120 min and acute mechanical stretch for 0, 30, 60, 120 min respectively. With Langendorff apparatus, an acute mechanically stretched heart model was established. There was no significant difference in the expression of TREK-1 among single Langendorff perfusion groups (P>0.05). As compared to non-stretched Langendorff-perfused heart, only the expression of TREK-1 in acute mechanically stretched heart (120 min) was greatly increased (P<0.05). This result suggested that some course of mechanical stretch could up-regulate the expression of TREK-1 in left ventricle. TREK-1 might play an important role in mechanoelectric feedback, so it could reduce the occurrence of arrhythmia that was induced by extra mechanical stretch.
Subject(s)
Feedback , Heart Ventricles/metabolism , Mechanotransduction, Cellular , Potassium Channels, Tandem Pore Domain/metabolism , Random Allocation , Rats, Wistar , Stress, MechanicalABSTRACT
To explore the role of mechanosensitive potassium channel TREK-1, Western blot analysis was used to investigate the expression changes of TREK-1 in left ventricle in acute mechanically stretched heart. Forty Wistar rats were randomly divided into 8 groups (n=5 in each group),subject to single Langendorff perfusion for 0, 30, 60, 120 min and acute mechanical stretch for 0, 30,60, 120 min respectively. With Langendorff apparatus, an acute mechanically stretched heart model was established. There was no significant difference in the expression of TREK-1 among single Langendorff perfusion groups (P＞0.05). As compared to non-stretched Langendorff-perfused heart, only the expression of TREK-1 in acute mechanically stretched heart (120 min) was greatly increased (P＜0.05). This result suggested that some course of mechanical stretch could up-regulate the expression of TREK-1 in left ventricle. TREK-1 might play an important role in mechanoelectric feedback,so it could reduce the occurrence of arrhythmia that was induced by extra mechanical stretch.
ABSTRACT
The expression of stretch-activated potassium channel TREK-1 mRNA and protein of hypertrophic myocardium was measured. Using a model of hypertrophy induced by coarctation of abdominal aorta in male Wistar rats, the expression of TREK-1 mRNA and protein was detected by using semi quantitative RT PCR and Western blot respectively. At 4th and 8th week after constriction of the abdominal aorta, rats developed significant left ventricular hypertrophy. As compared to sham operated group, stretch activated potassium channel TREK-1 mRNA was strongly expressed and protein was up regulated in operation groups (P＜0.05). It was concluded that the expression of TREK 1 was up regulated in hypertrophic myocardium induced by chronic pressure overload in Wistar rats.