Subcellular bases of cardiac disturbance in experimental informational neurosis

In experimental informational neurosis, accompanied by the development of stable arterial hypertension, tachycardia and dystrophic alterations in myocardium, the contractile protein ability to generate force and produce work as well as the power of the contractile process are significantly decreased and so is the intensity of Ca2+ transport through membranes of sarcoplasmic reticulum and mitochondria. Ca2+ content in these structures and energetic supply to the cardiac muscle do not change as compared with the control. Noradrenaline content in myocardium increases 5-fold compared with the control and 2.5-fold compared with the norm, while blood content falls to zero (sympathetic neuro-muscular contact is 'locked up' for noradrenaline outflow into the blood); dopamine content increases. Adenylate cyclase sensitivity to the stimulating effect of noradrenaline and NaF diminishes. Basal activity of phosphodiesterase increases, and its sensitivity to the inhibitory action of high calcium concentrations decreases. The disturbance in these systems may, on the one hand, be due to neural effects, and pressure overload of the heart, on the other hand, to the sharp rise in noradrenaline content in the myocardium and the change in the activity of cyclic adenosine monophosphate enzymes. It is suggested that similar changes may take place in the human myocardium and may underlie the cardiac weakness.