[Mechanisms of neurogenic dystrophies induced by activation and deprivation of the sympathetic nervous system].

Entry of abnormal nervous stimuli after sciatic nerve transection proved to affect the functioning of renal mineralocorticoid receptors as a result of inadequate neurotrophic support of this organ. Drug blockade of both neural and humoral transmission of the abnormal stimuli from the injured nerve to the kidney prevented development of trophic disorders as indicated by the status of the renal mineralocorticoid receptor system. At the same time, drug stimulation of the sympathetic nervous system further affected aldosterone reception by this organ.

[Effect of beta-adrenergic blocker propranolol during reflex renal degeneration induced by sciatic nerve transection].

We present the data on functional status of the mineralocorticoid receptor system in rat kidney in the course of renal reflex degeneration induced by sciatic nerve transection at the background of both renal denervation and injections of beta blocker propranolol. According to the status of renal mineralocorticoid receptors, simultaneous blocking of both neural and humoral pathological stimuli incoming to the kidney after the nerve injury to a higher extent inhibited cytochemical changes in the organ as compared to blocking the neural transmission alone. We propose that both the central neural transmission and humoral mechanisms control the activity of the molecular structures responsible for aldosterone reception in renal tubular cells.

[Aldosterone binding by compensatory hypertrophic kidney with disturbed neurotrophic supply in rats].

We studied certain aspects of interaction between (3H)aldosterone and the cytoplasmic as well as nuclear receptors of renal cells in the rats during compensatory renal hypertrophy at the background of reflex renal dystrophy. The dystrophy developing in the kidney after cutting the sciatic nerve blocks the compensatory increase in specific accumulation of (3H)aldosterone in the cytoplasm of the renal tubular cells. (3H)Aldosterone transport from the cytoplasmic receptors to the nuclear receptors during rat reflex dystrophy of compensatory hypertrophied kidney is lower as compared to the control.

[Influence of unilateral nephrectomy on aldosterone receptors in the remaining kidney in rats].

It was shown that the 30th day of compensatory kidney hypertrophy arising as a result of unilateral nephrectomy was accompanied by an increased binding of the mineralocorticoid hormone aldosterone by cytoplasmic receptors of the tubule cells of the remaining kidney. The transfer of aldosterone from cytoplasmic receptors to the nuclear receptors increased in the tubule cells of the hypertrophied kidney. This suggests that at the early stages hypertrophies are expressed as adaptive phenomena and phenomena related to intensified functioning of the organ fulfilling the double load.

[The role of beta-adrenoreceptors in pathogenesis of neurogenic dystrophies].

Sciatic nerve damage led to a defective functioning of the renal mineralocorticoid receptors due to the disturbed neurotrophic supply of this organ: the reception of distorted nervous stimuli. The pharmacological blockade of both the neurotransmitter and the humoral pathways of the pathological stimuli from the damaged nerve to the kidney prevented the development of trophic disturbances as tested by the state of the renal mineralocorticoid receptor system. At the same time, the pharmacological stimulation of the sympathetic nervous system leads to an even more defective aldosterone reception by the kidney.

[Binding of aldosterone with cytoplasmic and brain nuclear corticosteroid receptors in rats with various types of behavior].

The results are given of in vivo experiments on the binding of (3H)aldosterone to corticosteroid receptors of the cytoplasm and nuclei in the brain structure in rats with different types of behavior. Differences were established in binding (3H)aldosterone to corticosteroid receptors of the hippocampus cytoplasm in the animals with different types of behavior both under the normal conditions and within two weeks after stress. Stress was shown to affect the binding of this hormone to corticosteroid receptors of the brain cytoplasm (without hippocampus and cerebellum).

[Effects of stress and types of the animal behavior on the binding aldosterone with the brain corticosterone receptors].

Specific accumulation of 3H aldosterone by corticosteroid receptors of the brain structures was determined in in vitro and in vivo experiments on rats of different behavioral types under the normal conditions and within two weeks after stress. In both variants, stress decreased binding of 3H aldosterone to corticosteroid receptors of the rat brain. Differences were found in binding of 3H aldosterone to corticosteroid receptors of the hippocampus, rather than the whole brain, in animals with different behavioral types both under normal conditions and after stress.

[Receptor binding of aldosterone in the brain of rats with different types of behavior under normal conditions and after stress].

Results are given from experiments on binding of [3H]aldosterone to the cytoplasmic corticosteroid receptors, in the brain structures of the rat with different types of behavior under normal conditions 10 min and two weeks after its peritoneal injection. Binding of [3H]aldosterone to cytoplasmic corticosteroid receptors of the hippocampus, rather than the brain (without hippocampus and cerebellum), was shown to depend on the type of animal behavior. Stress was also shown to affect binding of this hormone to cytoplasmic corticosteroid receptors of the brain (without hippocampus and cerebellum), rather than hippocampus.

[The binding of [3H]aldosterone by brain corticosteroid receptors in rats with different individual-typological behavioral characteristics].

[3H]Aldosterone (AS) binding to cytoplasmic corticosteroid receptors (CR) of the hippocampus and brain (without cerebellum and hippocampus) was studied in rats of two behavioral types under normal conditions and within two weeks after electric-pain stress. No asymmetry was shown in the distribution of CRs that bound [3H]AS in the rats of both groups. A relationship was established between the hormone binding by CRs of the hippocampus, rather than the rest of the brain, and type of animal behavior.

[Aldosterone receptors of the rat kidney in sciatic nerve injury and various mechanisms for their regulation].

It was shown, that the lesion of the sciatic nerve leads to disturbance of functioning of mineralocorticoid receptors of kidneys, which was expressed primarily as deterioration of the Na+ reabsorption in the kidneys ductulus cells. Simultaneous pharmacological blockade by propranolol's injections of neuroconductive and humoral pathways of transmission to the kidneys of pathological stimulus, caused in result of chronic irritation of sciatic nerve, prevents the development of disturbance in kidney's mineralocorticoid receptor apparatus functioning to a more extent, than the blockade of the neuroconductive pathway only. The obtained results point out that propranolol is a substance, which may prevent the development of neurogenic dystrophies.

[The effect of the drug-induced activation and deprivation of the sympathetic nervous system on aldosterone receptor binding by the kidney with disturbed neurotrophic support].

The results of studies are presented on the determination of aldosterone accumulation by mineralocorticoid receptors on cytoplasm and nuclei of normal rat renal tubules as well as in disturbed neurotrophic supply of the kidney including that against the background of activation and deprivation of the sympathetic nervous system function. It was shown that a pharmacological stimulation of sympathetic nervous system potentiated functional disturbances of the renal mineralocorticoid receptor apparatus in reflex dystrophy of the kidney. A simultaneous pharmacological blockade both of neural and of humoral transmission of pathological stimuli from damaged sciatic nerve to the kidney prevented the development of these disturbances.

[The antidystrophic effect of the action of beta-adrenoblockaders in local damage to the nervous system].

It has been established that the lesion of the sciatic nerve, accompanied by a disturbance of normal neurotrophic provision of a kidney as a result of coming to the organ of the perverted nervous stimuli (by the neuro-conductive path through sympathetic nerves and by participation of the hypothalamus--hypophysis--peripheral glands system), leads to disturbance of functioning of mineral-corticoid receptors of kidneys. It has been also established that simultaneous pharmacological blockade of neuro-conductive and humoral pathways of transmission to the kidney of pathological stimuli from the central stump of the cut sciatic nerve prevents the development of trophic organ disturbances, tested by the state of the kidney mineral-corticoid receptor apparatus, while pharmacological stimulation of sympathetic nervous system leads to the greater disturbance of aldosterone reception by the cells of kidney channels. A valid conclusion can be made that propranolol is a substance, which may weaken possible non-adequate reactions of peripheral tissues to the action of physiologically active substances during the development of the consequences of the lesion of the nervous system and thus to prevent the development of neurogenic dystrophies.

[Sodium reabsorption and the aldosterone receptors in the cells of the kidney tubules in a dynamic disorder of the trophic function of the nervous system].

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.

[The mineralocorticoid receptor apparatus of the kidneys in rats with reflex dystrophy of the organ against a background of simultaneous denervation or blockade of the body beta-adrenoreceptors by propranolol].

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.

[Neurogenic dystrophy of the rat kidney and interaction of aldosterone with cytoplasmic and nuclear receptors of kidney tubules].

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.

[Reception of aldosterone by the rat kidney in its compensatory hypertrophy].

A study was made of the effect of the compensatory hypertrophy of the rat kidney (on the 30th day) on the interaction of 3H-aldosterone with the receptors of the kidney cell tubules. It has been shown that the compensatory hypertrophy of the kidney is accompanied by an increased intensity of 3H-aldosterone binding with the receptors of the nephron cell cytoplasm and a decrease of the transfer of the hormonoreceptor cytoplasm and 3 receptor complex to the nucleus. These changes in the mechanism of aldosterone reception by the hypertrophic kidney can be accompanied by disturbed sensitivity of the organ to this mineralocorticoid.

[Molecular mechanisms of the effect of neurogenic dystrophy of the kidneys in the rat on the sensitivity of the organ to aldosterone].

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.