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Biomedical subjects

V V Frol'kis

Publications and source records attributed to V V Frol'kis.

At least 19 recordsLinked to original sources
PubMed2004

[Mechanisms of nitric oxide activity in cardiovascular system as a basis of pathogenetic therapy of related diseases].

General characteristics and mechanisms of effects of nitric oxide (NO) and its role in the development of pathology are reviewed. Presented are the data about NO participation in the regulation of circulation and cardiovascular system; NO-dependent mechanism of regulation of cardiovascular reactivity against the background of dysfunction of endothelium; cGMP-independent mechanism of NO effect upon Ca homeostasis and the sensitivity of myofibrils of smooth muscle cells to Ca ions; pharmacological correction of disturbances of NO metabolism and related endothelial dysfunction; role of age changes of the endothelial function in the development of cardiovascular pathology.

Animals↗
PubMed1999

[Invertors--intracellular regulators of plasma membrane function].

It has been found that the activation of protein biosynthesis in various cells (hepatocytes, adrenocorticocytes, thyrocytes and myocardiocytes), caused by different factors such as multiple hormones, regeneration, hyperfunction etc., leads to the development of plasmatic membrane hyperpolarization. It has also been shown that during protein biosynthesis activation under genome control there have been synthesized the intracellular regulators of plasmatic membrane state, called invertors. The invertors regulate the activity of membrane enzymes and ion channels, as well as adapt plasma membrane state to the needs of cell. With increasing age, the invertors synthesis alters, and this becomes an important genome-membraneous mechanism of aging. An experimental lifespan prolongation promotes to maintain the synthesis of invertors.

Animals↗
PubMed1999

[Neurohumoral control of protein biosynthesis during aging].

It has been shown in the experiments on adult (6-8 mo) and old (26-28 mo) Wistar rats that in aging, due to an electrical stimulation of the hypothalamus, the liver induction of thyroxine aminotransferase, tryptophan-pyrrolase, glucose-6-phosphatase and fructose-1, 6-diphosphatase decreases. In old rats, the biosynthesis of RNA fractions gets activated at later periods. In contrast to adult animals, the electrical hypothalamic stimulation did not induce any marked changes in chromatin fractions ratio and transcriptional processes in old rats. With aging, it may happen that the target cells cannot respond to adequate stimulations, while the central (hypothalamic, in particular) mechanisms cannot realize them. In aging, the influence of the hormones (insulin, testosterone, thyroxin and hydrocortisone) on the synthesis of proteins-invertors, regulating plasmatic membrane state Is weakened. Following surgical denervation of the liver in old rats, the less marked changes in RNA and protein synthesis and lesser influences on monooxygenase induction were found in old rats. All these observations indicate an impairment of the neural control over protein biosynthesis in senescence. Also, the axonal transport of proteins is delayed in old rats that may influence the nervous cell aging. Owing to all these shifts, the plastic provision of body integrative reactions is impaired.

Aging↗
PubMed1998

[A model of chronic situational stress and its effect on the rate of aging and the longevity of rats].

In rat experiments a new model of situational chronic stress, with the use of multicomponent natural stimulating influences, has been elaborated. The study revealed two subpopulations with longer and shorter lifespan in the group of stressed rats vs. control group. The survival of stressed animals was correspondent with the changes of adaptive indices. Thus the situational chronic stress has the geropromotive or geroprotective effect which depends on the organism's adaptive capacities.

Adaptation, Physiological↗
PubMed1997

[The effect of olivomycin on the spontaneous regression of experimental atherosclerosis in rabbits of different ages].

Development and regression of experimental atherosclerosis in rabbits is an expressed age-related phenomenon, showing the increase in occurrence and pronouncement of atherosclerotic process with age. A new approach to the disease treatment by means of olivomycin is described. It has shown that while influencing considerably the protein biosynthesis of experimental animal, one can accelerate the regression of atherosclerosis by means of olivomycin and reduce protein and lipid metabolism indicators characterizing the disease development.

Aging↗
PubMed1993

[The role of invertors in the mechanism of heart function regulation].

Decrease of heart contraction function and rate, diminish of adreno- and fluoride-sensitivity of adenylate cyclase was detected under the long-time isolated rat's heart Langendorff's perfusion. Injection of rat with the Actinomycin D (an inhibitor of transcription) prevented the decline of hearts' function and adenylate cyclase activity. The addition of cytosol from cells of long-term perfused heart decreased the adrenosensitivity of adenylate cyclase of intact animal heart membranes. Actinomycin D prevented this effect. The appearance of cellular factor, which down-regulates adenylate cyclase activity (named by us an invertor) into the heart under the long-time perfusion is discussed.

Adenylyl Cyclases↗
PubMed1993

[The hypothalamic mechanisms of the development of arterial hypertension in old age].

The electrical activity of hypothalamic nuclei was found to change in accordance with changes in arterial blood pressure in old rabbits with reflexogenic hypertension. Stimulation of the hypothalamus induced an obvious increase in the blood pressure, considerable changes in cardiac activity, coronary insufficiency occurrence and alteration of the myocardium structure. An increase in excitability of the pressor structures of the anterior and posterior hypothalamic areas occurred with ageing. The age-induced changes in the hypothalamus could be either the primary mechanisms of development of hypertension, or they can be involved at later stages of the hypertension pathogenesis.

Aging↗
PubMed1992

[Membrane mechanisms of testosterone action].

The experiments on adult Wistar rats have shown that testosterone administration provoke hyperpolarization of hepatocytes and adrenocorticocytes plasmatic membranes. It was discovered that this hyperpolarization was caused by cell Na, K-ATPase activation. Inhibitors of protein biosynthesis prevent both testosterone-induced hyperpolarization and Na, K-ATPase activation. It is shown that some hyperpolarization factor appeared in the cytosol and blood serum under testosterone influence. It was suggested that this mechanism is mediated by cell genome.

Adrenal Cortex↗