CATECHOLAMINES MODULATE PROTEIN-TURNOVER IN CULTURED, QUIESCENT RABBIT CARDIAC MYOCYTES

When rabbit ventricular myocytes were cultured for 1 wk and then expos ed to alpha- and/or beta-adrenergic agonists, such nonbeating heart ce ll preparations disclosed increased protein-to-DNA ratios and elevated RNA content, indicative of cellular hypertrophy. Norepinephrine, isop roterenol, and phenylephrine provoked hypertrophy with norepinephrine eliciting a greater response than isoproterenol or phenylephrine. Spec ific alpha- and beta-antagonists blocked growth by inhibiting catechol amine-induced changes in protein turnover. Each catecholamine enhanced the fractional rate of protein synthesis within 48 h; however, change s in growth rates appeared to be modulated, in part, by alterations in protein degradation. Even though rates of total protein and actin syn thesis resembled values measured in vivo, myosin heavy chain fractiona l rate of synthesis was only 22% of in vivo levels. Double label immun ofluorescence microscopy further illustrated that catecholamine treatm ent accelerated myofibrillar disruption in these quiescent heart cells . These observations suggested that in the absence of beating, neurohu moral modulation of contractile protein turnover was not associated wi th the maintenance of myofibrillar integrity even though catecholamine s induced cellular hypertrophy.