Why the study?
Does amiloride reduce norepinephrine-induced protein synthesis in cultured neonatal rat cardiomyocytes?
Does amiloride reduce norepinephrine-induced protein synthesis in cultured neonatal rat cardiomyocytes?
Alpha 1-adrenergic stimulation enhances protein synthesis through activation of Na+/H+ exchange, suggesting Na+ influx and/or pH increase play a key role in cardiac hypertrophy.
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Amiloride attenuation of norepinephrine effects remains hypothesis-generating; leaves open in vivo role for Na+/H+ exchange inhibition in hypertrophy.
It is reported that Na+ influx contributes to stretch-induced cardiac hypertrophy. Na+ influx may also be involved in cardiac hypertrophy induced by catecholamine. In the present study, to test whether Na+/H+ exchange plays an important role in norepinephrine-induced cardiac hypertrophy, the effect of Na+/H+ exchange inhibitor, amiloride on protein synthesis was studied in cultured neonatal rat cardiomyocytes in serum free medium. [3H]Phenylalanine uptake was determined 24 and 48 hours after administration of norepinephrine with and without amiloride. In the control, norepinephrine increased [3H]phenylalanine uptake in a dose dependent manner (10(-5)-10(-7) M). Prazosin (10(-7) M) and amiloride (10(-5)-10(-4) M) significantly attenuated the norepinephrine mediated protein synthesis. These results indicate that alpha 1-adrenergic stimulation enhances the protein synthesis through activation of Na+/H+ exchange. Therefore, Na+ influx and/or PH increase may play a key role in cardiac hypertrophy.
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Hori et al. (1990) studied this question.
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