Alpha 1-adrenergic stimulation of rat myocardial cells increases protein synthesis.
The effects of adrenergic stimulation on the rates of protein synthesis, degradation, and accumulation were examined in primary cultures of neonatal rat heart cells. Treatment of myocardial cells with norepinephrine increased total cellular protein content and the rate of incorporation of radiolabeled tyrosine into trichloroacetic acid insoluble protein. alpha 1-Adrenergic, but not alpha 2- or beta-adrenergic blockade, inhibited these norepinephrine induced increases. The rate of protein synthesis estimated from the kinetics of equilibrium labeling and from combined equilibrium and pulse labeling was increased by norepinephrine stimulation, whereas protein degradation estimated by release of previously incorporated radiolabeled tyrosine or in pulse-chase experiments was unaffected. To determine whether alpha 1-adrenergic stimulation produced similar effects on the turnover of myofibrillar proteins, rates of synthesis and degradation were estimated for a myofibrillar-enriched protein fraction and for myosin heavy chain and actin. Norepinephrine treatment produced increases in the synthesis of myofibrillar protein without significantly altering degradation rates. These experiments suggest that alpha 1-adrenergic stimulation increases myocardial cell protein content by accelerating protein synthesis.
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D002478:Cells, Cultured; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D009210:Myofibrils / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D014176:Protein Biosynthesis; D011506:Proteins / Q000378:metabolism; D051381:Rats; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D013268:Stimulation, Chemical
D000596:Amino Acids; D011506:Proteins; D011942:Receptors, Adrenergic, alpha; D009638:Norepinephrine