Pressure and volume overload in pigs induced distinct growth factor activation, with pressure overload increasing angiotensinogen and ppET-1 mRNA by 13- and 112-fold versus sham at 3 and 6 hours.
Acute cardiac adaptation to pressure versus volume overload involves distinct temporal patterns of growth factor activation, which initially support contractility and subsequently induce hypertrophy.
To investigate the time sequence of cardiac growth factor formation, echocardiographic and hemodynamic measurements were performed at scheduled times, and mRNAs for angiotensinogen, prepro-endothelin-1 (ppET-1), and insulin-like growth factor I (IGF-I) were quantified with RT-PCR and localized with in situ hybridization in pigs (fluothane anesthesia) by use of pressure or volume overload (aortic banding and aorta-cava fistula, respectively). Relative peptide formation was also measured by radioimmunoassay. In pressure overload, angiotensinogen and ppET-1 mRNA overexpression on myocytes (13 times vs. sham at 3 h and 112 times at 6 h, respectively) was followed by recovery (12 h) of initially decreased (0.5-6 h) myocardial contractility. In volume overload, contractility was not decreased, the angiotensinogen gene was slightly upregulated at 6 h (6.7 times), and ppET-1 was not overexpressed. IGF-I mRNA was overexpressed on myocytes (at 24 h) in both volume and pressure overload (14 times and 37 times, respectively). In the latter setting, a second ppET-1 overexpression was detectable on myocytes at 7 days. In conclusion, acute cardiac adaptation responses involve different growth factor activation over time in pressure versus volume overload; growth factors initially support myocardial contractility and thereafter induce myocardial hypertrophy.
Modesti et al. (Fri,) conducted a other in Pressure- and volume-overload hypertrophy. Pressure or volume overload vs. Sham was evaluated on Cardiac growth factor formation (mRNAs for angiotensinogen, ppET-1, and IGF-I) and myocardial contractility. Pressure and volume overload in pigs induced distinct growth factor activation, with pressure overload increasing angiotensinogen and ppET-1 mRNA by 13- and 112-fold versus sham at 3 and 6 hours.