G proteins-coupled signaling pathways appear to play a role in the development of cardiac hypertrophy and its progression to heart failure. The present study aimed to investigate trimeric G proteins and adenylyl cyclase signaling in immature as well as in adult rat myocardium during this process caused by pressure overload. Pressure overload was induced in newborn (2-day-old) rats by abdominal aortic banding and myocardial preparations from left ventricular myocardium of immature (10-day-old) and adult (90-day-old) animals were analyzed for the relative content of different G protein subunits and adenylyl cyclase (AC) by immunoblotting with specific antibodies. A functional status of the AC signaling system was also evaluated. Normal maturation of rat heart was accompanied by increased expression of AC type V/VI and VII and of the long isoform (G(s)alphaL) of G(s)alpha protein. In parallel, the amounts of myocardial G(i)alpha/G(o)alpha proteins tended to decrease, and G(q)alpha/G(11)alpha and Gbeta did not change. Interestingly, whereas fluoride-stimulated AC activity increased in the course of maturation, activity of AC measured under other experimental conditions (stimulation by Mn2+, forskolin or isoproterenol) was lower in adult than in young rat myocardium. Pressure overload did not influence distribution of G proteins in immature myocardium, but considerably decreased the content of G(s)alphaL and increased G(o)alpha proteins in hearts of 90-day-old rats. These hearts exhibited worsened functional reserve as compared to age-matched controls and activity of AC was also markedly lower. A considerable reduction in Mn(2+)-stimulated AC activity together with similar decrease in AC activity determined under other stimulation conditions suggests that it is a function of AC catalytic subunit that is primarily impaired in this model of pressure overload.

• MeSH
• Adenylyl Cyclases genetics   metabolism   MeSH
• Gene Expression MeSH
• Fluorides pharmacology   MeSH
• Hypertrophy, Left Ventricular metabolism   MeSH
• Isoproterenol pharmacology   MeSH
• Cardiomegaly genetics   metabolism   pathology   MeSH
• Cardiotonic Agents pharmacology   MeSH
• Colforsin pharmacology   MeSH
• Rats MeSH
• Manganese pharmacology   MeSH
• Myocardium metabolism   MeSH
• Animals, Newborn * MeSH
• Rats, Wistar MeSH
• Protein Isoforms genetics   metabolism   MeSH
• GTP-Binding Proteins metabolism   MeSH
• Signal Transduction MeSH
• Aging MeSH
• Pressure * MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Comparative Study MeSH
• Names of Substances
• Adenylyl Cyclases MeSH
• Fluorides MeSH
• Isoproterenol MeSH
• Cardiotonic Agents MeSH
• Colforsin MeSH
• Manganese MeSH
• Protein Isoforms MeSH
• GTP-Binding Proteins MeSH