Abstract

Organic exposure to various forms of stress creates a mechanism of adjustment to maintain the changes of internal environment to the minimum and to secure a rapid resumption which comes into operation for the homeostatic adaptation. The autonomic nervous system does seem to play a major role in such a mechanism. It is of our interest to assess the reaction of the organism through urinary excretion of catecholamines during an induced disturbance of the equilibrium of the autonomic nervous system.When adrenaline was loaded in patients with various diseases, urinary excretion of adrenaline increased by approximately 2% of the administered dose, while noradrenaline administration resulted in the urinary excretion of 1.3% of the administered noradrenaline. In each case, no significant correlation was noted between such increases in urinary excretion and renal function tested by PSP excretion or liver function by BSP retention. Urinary excretion of catecholamine appeared not to be affected by the hepatic and renal dysfunction, but to reflect blood catecholamine level approximately.Urinary excretion of noradrenaline had decreased after adreanaline loading. A significant correlation was seen between the absolute value of the decrease in urinary excretion of noradrenaline and urinary noradrenaline excretion before adrenaline administration (r=0.90), probably indicating a compensation mechanism of the adrenaline action for the sympathetic discharge.A positive correlation was found between the increase in urinary excretion of noradrenaline upon noradrenaline administration and the level of urinary excretion of noradrenaline of control period (r=0.71). Urinary excertion of adrenaline also increased upon noradrenaline administration, showing a positive correlation with adrenaline excretion before noradrenaline administration (r =0.75).Such increase in urinary excretion of adrenaline and decrease in urinary excretion of noradrenaline upon adrenaline administration as well as inverase in urinary excretion of both adrenaline and noradrenaline upon noradrenaline administration were also seen in experiments in rabbits. Noradrenaline loading in reserpinized rabbits also resulted in increases in urinary excretion of adrenaline and noradrenaline to the same extent as in control rabbits receiving noradrenaline alone. Increase in urinary excretion of adrenaline upon noradrenaline administration probably indicates the synthesis of adrenaline in vivo from the administered noradrenaline.In order to see what happens to the catecholamine secretion, the parasympathomimetic agent such as pilocarpine or neostigmine was administered into the patients with thyrotoxicosis and atrial septal defect as well as the normal subjects, because urinary excretion of catecholamine has been found to increase in these patients. The urinary excretion of catecholamine increased remarkably in thyrotoxicosis but less significantly in atrial septal defect and normal subjects, while the administration of atropine, parasympatholytic agents, caused a decrease in urinary excretion of catecholamine proportional to its previous urinary level. Administration of neostigmine in rabbits caused a significant increase in urinary excretion of catecholamine. However, pretreatment with hexamethonium bromide resulted in an inhibition of the effect of neostigmine administration. From these results, it was presumed that the increase in urinary excretion of catecholamine upon administration of the parasympathomimetic agent is based upon the excitation of the sympathe-tic nervous system.

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