Acute right ventricular pressure overload and Na+ influx in cardiocytes rapidly enhanced Na(+)-Ca2+ exchanger expression and accelerated protein synthesis, hallmarks of cardiac hypertrophy.
Acute cardiac pressure overload and Na+ influx rapidly upregulate Na(+)-Ca2+ exchanger expression and stimulate protein synthesis, representing early events in cardiac hypertrophy.
This report identifies a rapid increase in the expression of cardiac Na(+)-Ca2+ exchanger mRNA in response to an acute pressure overload. This enhanced exchanger expression appeared within 1 h after the onset of right ventricular pressure overload in the cat and was sustained during cardiac overloading for at least 4 h. Maintenance of this right ventricular pressure overload for 48 h evoked an increase in the production of exchanger protein. Because of our previous finding that load imposition on the heart initiates cell growth and our hypothesis that this is in response to the enhanced entry of cellular cations, we then examined the effect of Na+ influx into cultured adult cardiac myocytes, or cardiocytes, in terms of early anabolic responses. Pressure overload of the heart and cardiocyte Na+ influx were found to produce a common, rapid result in terms of both enhanced Na(+)-Ca2+ exchanger expression and accelerated synthesis of general and contractile proteins, the hallmarks of cardiac hypertrophy.
Kent et al. (Wed,) conducted a other in Cardiac pressure overload. Right ventricular pressure overload and Na+ influx was evaluated on Expression of cardiac Na(+)-Ca2+ exchanger mRNA and protein, and synthesis of general and contractile proteins. Acute right ventricular pressure overload and Na+ influx in cardiocytes rapidly enhanced Na(+)-Ca2+ exchanger expression and accelerated protein synthesis, hallmarks of cardiac hypertrophy.
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