PubMed Health⌕ Search

Biomedical subjects

Ia I Azhipa

Publications and source records attributed to Ia I Azhipa.

At least 37 records · Page 2Linked to original sources
PubMedDate not supplied

[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.

Aldosterone↗
PubMedDate not supplied

[Changes in the serotonin metabolism of rats with neurodystrophic process].

Some mechanisms of alteration in serotonin content in tissues and an effect of the amine on development of visible trophic impairment in rats were studied under conditions of neurodystrophic impairments which occurred in the animals as a result of chronic stimulation of sciatic nerve. A long-term increase in serotonin content in tissues of rats with the neurodystrophic process was due to activation of its synthesis. Elevation in serotonin content in animals under conditions of chronic stimulation of peripheral nervous system might be of importance for development of neural and neurogenic dystrophies.

5-Hydroxytryptophan↗
PubMedDate not supplied

[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.

Adaptation, Physiological↗
PubMedDate not supplied

[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. 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.

Aldosterone↗