Abstract
Addition of epinephrine in vitro to incubating slices of rat heart left ventricle did not influence the rate of protein synthesis as determined by the rate of incorporation of L-[3H]leucine into the slice proteins. Injections of suspensions of epinephrine, norepinephrine, isoproterenol or phenylephrine in oil subcutaneously into rats, however, caused an increase in the rate of protein synthesis in ventricle slices from these animals. Isoproterenol had the greatest and phenylephrine the smallest effect. A single injection of 1 mg/kg of epinephrine or norepinephrine resulted in increased protein synthesis in five hours. The magnitude of increase was a function of the dose and the number of injections. The data suggest that chronic exposure of the heart to high levels of endogenous catecholamines may result in increased cardiac protein synthesis and ultimately in cardiac hypertrophy. The effect of these agents on protein synthesis may occur indirectly in response to catecholamine-induced cellular damage or as a consequence of increased cardiac contractility, rate or output promoted by them in vivo due to interaction with cardiac beta receptors. Propranolol inhibited the stimulating effects of isoproterenol and epinephrine on protein synthesis considerably. However, the mechanism may be more complex since alpha adrenergic blocking agents also reduced the effect of norepinephrine. Depletion of tissue catecholamines in rats by reserpine plus adrenal demedullation or adrenalectomy did not reduce rates of protein synthesis. Hence normal tissue levels of catecholamines may not be required for maintenance of normal rates of cardiac protein synthesis.
Footnotes
- Received June 19, 1972.
- Accepted July 20, 1973.
- © 1973 by The Williams & Wilkins Co.
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