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Excretion of catecholamines and DOPA was impaired in patients with metabolic-alimentary obesity, with ischemic disease of heart, with atherosclerosis and excessive weight. Distinct decrease in content of adrenaline, noradrenaline and DOPA was observed in patients with obesity; the phenomenon was less pronounced in ischemic disease of heart, mainly in aged patients. Correlation was found between the rate of excretion of catecholamines and DOPA and the extent of hyperlipidemia. Dietetics did not normalize completely the impairments studied. Additional administration of pyridoxine caused a favorable effect.

After a single administration of norepinephrine or DOPA to albino rats there occurred an incorporation of norepinephrine into the adrenergic axons of the heart and its deposition in the form of granules in small synaptic vesicles, about 300 A in diameter. The adrenergic and cholinergic axons can be thus differentiated. The amount of cholinergic axons in the auricles is greater than that of the adrenergic ones. The adrenergic terminals came into the most intimate contact with the cholinergic terminals and with the endothelial cells of the blood capillaries and the myocardial muscle cells. It is supposed that adrenergic fibers can act upon the heart muscle in three ways: by means of presynaptic inhibition through the cholinergic axons, by humoral route, and directly on the myocardial muscle cells.

It was shown that administration of noradrenaline precursor--L-DOPA (45 mg/kg) to pregnant adrenal- or ovariectomized rats restored the reaction of their fetuses to stress to the level characteristic of fetuses, whose mothers were falsely operated with their adrenal glands and ovaries remaining in situ. It is supposed that during the prenatal development in rats stress-reaction was realized with the participation of noradrenaline of the maternal CNS.

The authors examined the changes in arterial blood pressure and the content of Noradrenaline in the myocardium, brain and aorta of rats with hypertension due to nephrectomy and treatment with desoxycorticosterone and NaCl, and after a chronic 6-month treatment of hypertension with various antihypertensive means. The most significant reduction of noradrenaline in the three of the examined tissues was found in rats, which received dic. sulfyram (100 mg/kg per os). Clondine (10 mkg/kg, per os) manifested the strongest hypotensive effect and lowered the level of noradrenaline in the myocardium, while it was raised in the aorta. Reserpine (10 mkg/kg, s. c) induced a clear reduction of Noradrenaline content in the brain, but an increase in the other two tissues. Insignificant hypotensive effect was observed in animals, treated with guanetidine (0.5 mg/kg, per os), which did not affect substantially noradrenaline in the examined organs. The increase of noradrenaline level was established in the three of the organs of animals, treated with alpha-methyl-DOFA (25 mg/kg, per os). Furosemide (1 mg/kg, s.c.) induced a statistically significant elevation of noradrenaline in the aorta, but was noneffective to noradrenaline in the myocardium and brain.