Dynamics of the rate of protein synthesis in sympathetic neurons as a factor determining the hyperfunction and hypertrophy of the heart

Abstract

The dynamics of the rate of protein synthesis (as shown by incorporation of [ 3H]lysine) in sympathetic neurons of stellate ganglia innervating the heart during protracted hyperfunction was investigated by the method of autoradiography. The dynamics of the noradrenaline content in the myocardium was determined biochemically. The sympathetic nerve fibres in the myocardium were demonstrated by histochemical (fluorescent) method and their number was estimated. Hyperfunction of the heart produced by aortic stenosis was accompanied by intense activity of the innervating sympathetic neurons involving changes in all the measured indices. In the stage of acute damage (4 to 7 days following the onset of heart hyperfunction) activation of protein synthesis in the cytoplasm and the nuclei of sympathetic neurons was observed together with a subnormal content of noradrenaline in the myocardium. In the next stage of relatively stable hyperfunction, the intensity of protein synthesis in the neurons was normal but the content of noradrenaline in the hypertrophied myocardium was reduced. In the third stage of exhaustion of the myocardium, 6 months after the onset of hyperfunction of the heart, the intensity of synthesis in the sympathetic neurons was inhibited twofold, the content of noradrenaline in the myocardium was reduced by 4 to 5 times and the number of histochemically determined adrenergic fibres in the myocardium was decreased by about 3 times. Thus in the process of hyperfunction of the sympathetic neurons regulating the activity of this intensely working organ, 3 stages of reaction of the apparatus of protein synthesis to the increase of physiological function were distinctly manifested. The first stage of activation of synthesis is the basis of neuronal adaptation to the increased load, and the final stage of inhibition of synthesis is the cause of functional insufficiency of the neuron and its structural atrophy.