Cardiomegaly induced by pressure overload in newborn rats is accompanied by altered expression of the long isoform of Gsα protein and deranged signaling of adenylyl cyclase

摘要: G proteins-coupled signaling pathways appear to play a role in the development of cardiac hypertrophy and its progression heart failure. The present study aimed investigate trimeric proteins adenylyl cyclase immature as well adult rat myocardium during this process caused by pressure overload. Pressure overload was induced newborn (2-day-old) rats abdominal aortic banding myocardial preparations from left ventricular (10-day-old) (90-day-old) animals were analyzed for relative content different protein subunits (AC) immunoblotting with specific antibodies. A functional status AC system also evaluated. Normal maturation accompanied increased expression type V/VI VII long isoform (GsαL) Gsα protein. In parallel, amounts Giα/Goα tended decrease, Gqα/G11α Gβ did not change. Interestingly, whereas fluoride-stimulated activity course maturation, measured under other experimental conditions (stimulation Mn2+, forskolin or isoproterenol) lower than young myocardium. influence distribution myocardium, but considerably decreased GsαL Goα hearts 90-day-old rats. These exhibited worsened reserve compared age-matched controls markedly lower. considerable reduction Mn2+-stimulated together similar decrease determined stimulation suggests that it is function catalytic subunit primarily impaired model