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Ia I Azhipa

Publications and source records attributed to Ia I Azhipa.

At least 19 recordsLinked to original sources
PubMed1978

[Electron paramagnetic resonance study of the products of the reaction between nitrogen oxides and several organic compounds].

A method of electron paramagnetic resonance was applied to the study of a possibility of paramagnetic centres formation in the nitrogen oxide reaction with saturated and unsaturated fatty acids and aromatic amino acids. Several paramagnetic centres are formed in interaction of NO2 with oleic acid at 20 degrees C. Saturated fatty acids formed no paramagnetic centres in the reaction with NO2. NO formed no paramagnetic centres not only with butyric, palmitic, and stearic acids, but also with oleic acid. The capacity of NO2 to form paramagentic centres with tyrosine in its saturated solution was revealed. In case of interaction between NO and NO2 with saturated phenylalanine and tryptophane solutions no formation of paramagnetic centres was observed. It is suggested that unsaturated fatty acids and tyrosine remnants of the membrane lipoprotein complexes could serve as peculiar targets with which NO2 interacted, and that formation of paramagnetic centres in the NO2 reaction with the mentioned substances was the primary act of the membrane damage.

Amino Acids↗
PubMedDate not supplied

[Cyclic AMP in the kidneys of adrenalectomized and nonadrenalectomized normal rats and rats with reflex dystrophy against a background of organ denervation and a total block of the body's beta-adrenoreceptors by propranolol].

Using the radioimmunological assay, renal cAMP content was studied in adrenalectomized and non-adrenalectomized rats with reflex dystrophy resulting from chronic ischiatic nerve stimulation against the background either of organ denervation or of general beta-adreno-blockade with propranolol. It was shown that the surgical denervation of kidney resulted in an increase in renal cAMP both in norm and especially in reflex dystrophy. The beta-adrenoceptor blockade with propranolol was accompanied by a decrease in renal nucleotide being more pronounced in animals with intact ischiatic nerve. Based on own and literature data we have suggested that one cause for the damage to renal aldosterone receptors in reflex dystrophy under pathological stimulation from the focus of damage in ischiatic nerve as well as for their improved functioning in surgical or pharmacological (beta-adrenoceptor blockade) desympathization which discontinues this stimulation, may be change in cAMP content. Via cAMP-dependent protein kinases, this nucleotide triggers a complex system of intracellular metabolic transformations which is able to change the protein spectrum of cytoplasm, nucleus, and chromatin and, therefore, the protein complex of aldosterone receptors. A participation of other biochemical systems of aldosterone stimulus transmission, including cAMP-independent ones, in processes of damage and normalization of tubule cells of the kidneys undergoing reflex dystrophy cannot be excluded.

Adrenal Glands↗
PubMedDate not supplied

[The effect of different body allowances of aldosterone on serotonin and cAMP metabolism in the tissues of rats with a disordered trophic function of the nervous system].

Effect of aldosterone on the content of serotonin, cAMP, and the activity of 5-hydroxytryptophane decarboxylase was studied in different rat tissues (hypothalamus, kidneys, tibial muscles) in norm and following the lesion of sciatic nerve in nonadrenalectomized and adrenalectomized animals, that is in conditions of severe deficiency of endogenous aldosterone. In nonadrenalectomized rats, exogenous aldosterone exerted either very little effect or no effect on the tissues metabolism of serotonin and cAMP. Aldosterone induced changes in the content of considered substances against the background of adrenalectomy in animals with intact sciatic nerve. These changes were observed usually only in hypothalamus and kidneys and reached their peak 60 or 90 min following the aldosterone administration. The changes in serotonin and cAMP tissues metabolism under the chronic stimulation of nervous system periphery with aldosterone may be an additional factor which enables further aggravation of trophic state of tissues and organs and alteration of their sensitivity to hormones, in particular, aldosterone.

Adrenalectomy↗
PubMedDate not supplied

[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.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

[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.

Aldosterone↗
PubMedDate not supplied

[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.

Absorption↗