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The results are presented of investigations on determining the functional state of mineralocorticoid receptor apparatus in rat kidney at diverse stages of the reflex renal dystrophy per se and that against the background of renal denervation along with propranolol injections produced at different terms following the disturbance of nervous system trophic function. It was shown that simultaneous blockade of neuroconductory and humoral pathways of pathological stimulus transmission from central end of cut ischiatic nerve to the kidney prevents the development of trophic disturbances in the organ as tested by the state of mineralocorticoid receptors, to a more extent than the blockade of neuroconductory pathway only. The activity of molecular structures which determine the mineralocorticoid reception in cells of renal tubules seems to be controlled both by central neuroconductory and humoral mechanisms.

Interaction of labeled aldosterone with rat kidney mineral corticoid cytoplasm receptors and duct cell nuclei at different dysfunctions of nervous-trophic organ supply. Dysfunction of vagus innervation leads to breakage of cytoplasm receptor apparatus and duct cell nuclei that performs aldosterone reception. Organ denervation and introduction of beta-adrenoblocking agent prevents development of kidney neurogenous dystrophy.

The effect of reflex and denervated dystrophy of the rat kidneys on the interaction of aldosterone-3H with specific cytoplasmic receptors and nuclei of this organ was investigated in vitro and in vivo experiments. It was found that reflex dystrophy decreases the intensity of hormone binding with cytoplasmic receptors by 36% and aldosterone-3H accumulation in the renal nuclei by 51%. The influence of denervated dystrophy of the organ specific hormone accumulation in the same subcellular fractions was not observed. The more accurate data on the effect of renal reflex dystrophy on aldosterone-3H-receptor interaction were obtained in vivo experiments comparatively to those in vitro.

Dystrophy of rat kidney caused by denervation did not affect the binding of 3H-aldosterone with specific receptors of cytoplasm and nuclei in the small tubular cells. But under conditions of reflectory dystrophy the rates of 3H-aldosterone binding with cytoplasm receptors as well as the hormone transmission from cytoplasmic to nuclear receptors were decreased. The impairments observed in molecular mechanisms of the aldosterone consumption in kidney tubular cells may be responsible for alterations in the tissue sensitivity to the hormone, which was expressed primarily as deterioration of the Na+ reabsorption in the neurodystrophic injury.