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Iu V Postnov

Publications and source records attributed to Iu V Postnov.

At least 19 recordsLinked to original sources
PubMed1992

[Effects of La3+ on calcium binding to erythrocyte cytoskeleton].

When the whole erythrocytes were exposed to LaCl3, A--23187, ionomycin, orthovanadate and saponin, there was Ca2+ binding only following La3+ treatment of the cells. The binding was evident at a wide range (0.1 microM--1.OmM) of La3+ concentrations. Iodoacetamide-induced (incubation for 3 hours, 37 degrees C) decrease in erythrocyte ATP levels was found to result in a 3-fold reduction in Ca2+ binding to the cytoskeleton. La(3+)-induced Ca2+ binding enhanced the incorporation of 14C-glucose and/or its metabolites into the red cell skeleton. Thus, the detected new type of Ca2+ binding to the cytoskeleton of human and rat erythrocytes is likely to be due to the cumulative process: direct binding of La3+ to the outer surface of a membrane and the metal-induced trigger of nucleotide--dependent intracellular process.

Adenosine Triphosphate↗
PubMed1991

[Calcium binding to the erythrocyte cytoskeleton in spontaneously hypertensive rats].

The paper outlines a new La(3+)-induced mechanism of Ca2+ binding to rat red blood cells. Other compounds elevating intracellular Ca2+ concentrations, such as A-23187, ionomycin, and orthovanadate, and some activators of phosphotransferases (TPA, dibutyryl cAMP) fail to initiate the binding. Inhibitors of calmodulin-dependent processes, such as calmidazolium and trifluoroperazine, diminish La-dependent Ca2+ binding. La(3+)-induced Ca2+ binding is followed by an increased cytoskeleton incorporation rate of 14C metabolites of glucose. The rate of Ca2+ binding and 14C metabolite incorporation was 30% and 80% higher, respectively, but Ca+ binding capacity was increased by 45% in SHR as compared to WKY rats. Due to the fact that La3+ enhances the phosphorylation of proteins with molecular masses of 14, 36, and 58 kD, it is suggested that Ca2+ binding alterations should be determined by changes in phosphorylation and glucose metabolic disturbances in spontaneously hypertensive rats.

Animals↗
PubMed1991

[Diagnostic value of the endomyocardial biopsy in the cardiologic therapeutic clinic].

Literature and authors' own data on the diagnostic value of endomyocardial biopsy in cases with clinical diagnosis of dilatation cardiomyopathy are analysed. It is shown that due to this biopsy the diagnosis of more than 20 heart diseases becomes possible. Myocarditis, the diagnosis of which is particularly difficult, is most frequently masked under dilatation cardiomyopathy. Ultrastructural studies are of great importance allowing to diagnose a number of heart diseases including alcoholic cardiomyopathy and viral myocardial lesions. The authors advocate wider use of endomyocardial biopsy which is sufficiently safe and informative.

Adult↗
PubMed1989

[C-src locus determines increased rate of Na+,K+-cotransport and increased calcium content in erythrocytes of (SHR x WKY) F2 hybrids].

26 male F2 hybrids between spontaneously hypertensive (SHR) and normotensive control (WKY) rats (SHRxWKY)F2 were segregated according to their c-src genotype into SS and WW homozygous groups, corresponding to SHR or WKY and WS heterozygous group. Na, K cotransport in erythrocytes in the WW group was equal to that of WKY and differs significantly from that of WS and SS groups (the rate of Na, K cotransport in latter groups was close to that of SHR). Ca content of RBC in WW group was equal to that of WKY, lower than that of WS and SS groups which in turn was significantly lower than in SHR, indicating polygenic control of the trait. Authors conclude that the c-src locus itself or some other loci inherited in conjunction with c-src determines both the increase of Na, K cotransport and calcium content in erythrocytes of SHR.

Animals↗
PubMed1989

[Transport of monovalent cations and calcium in erythrocytes of rats with spontaneous hypertension: study with fractions enriched with young and old cells].

The erythrocytes from two spontaneously hypertensive rat strains (SHR and MHS) differ from those of control strains such as WKY and MNS in showing lower values of the mean volume and higher Na,K-cotransport rates. After 4-hour incubation in the presence of orthovanadate 45Ca levels in the erythrocytes from SHR was twice as high as in those from WKY. Under the same conditions, hemoglobin crystallization occurred, this process in SHR erythrocytes took place more intensively. No difference was found in these parameters between MNS and MHS. The fractions enriched with young and old cells remained to display variations in the mean volume of cells, Na,K-cotransport rates, 45Ca levels and hemoglobin crystallization, which were recorded between SHR and WKY. The WKY-SHR hybrids of second generation indicated that only Na,K-cotransport rates of the parameters examined positively correlated with blood pressures. From the findings it was concluded that the differences in the volume of erythrocytes and their permeability for cations were not due to the changed time course of cell aging in the blood bed, but to the specific characteristics of cytoskeleton protein arrangement, which were primarily typical of a rat reticulocytic membrane.

Animals↗
PubMed1989

[A new stage in the development of the membrane concept of the pathogenesis of primary hypertension: the role of cellular oncogenes in the genesis of membrane disorders].

The membrane concept of the primary (essential) hypertension pathogenesis considers the start of the disease as being linked to the characteristic disturbances of the cation-transport function. The membrane alteration result in the increase of the free calcium ion concentration in the cell cytoplasm and are the cause of both the contractile properties alteration of the vascular smooth muscle cells and the alteration of the neuromediator release in the nerve endings. The further stage in the evolution of this concept was the observation of the pathogenetic ling between the membrane "defect" in the primary hypertension and the alteration of the cell oncogenes (proto-oncogenes) function. The presence of such a link may be confirmed by both the indirect proofs considered in the paper and the results of the DNA study in rats with a spontaneous hypertension by method of RFLP analysis.

Animals↗
PubMed1989

[Protein kinase C activity in the brain tissue of spontaneously hypertensive rats].

Protein kinase C activities in the brain tissue of spontaneously hypertensive rats (SHR) and normotensive control rats (WKY) were studied. Protein kinase C activity in SHR was found to be 35% higher than that in normotensive control rats. It is suggested that the increase in protein kinase C activity is involved in the mechanism of membrane alterations in primary hypertension.

Animals↗
PubMed1988

[Univalent cation transport in human and rat erythrocytes: its regulation by protein kinase activators and compression].

The effect of the activators of protein kinase A (dibutyryl-cAMP) and protein kinase C (beta-phorbolic ether), as well as cell compression, on the rate of 22Na and 86Rb, a radioactive potassium analogue, incorporation by human and rat erythrocytes was investigated. Protein kinase A and protein kinase C activation was accompanied by the activation of Na+, K+-ATP-ase in human and rat erythrocytes as well as increased Na+, K+ cotransport rate in rat erythrocytes. Human erythrocytes responded to protein kinase C activation by a 2 or 3-fold increase in Na+/Na+-antitransport rate, and both human and rat erythrocytes exhibited a manifold increase in the Na+/H+ metabolism rate. Cell compression depressed Na+, K+-ATP-ase activity and increased the rates of Na+/H+ metabolism and the frusemide-inhibited component of potassium transport, the latter two effects being particularly obvious in rat erythrocytes. It is suggested that protein kinase C activation and/or erythrocyte compression may be a direct cause of increased plasmatic membrane permeability for univalent cations in primary hypertension.

Animals↗
PubMed1988

[Regulation of the shape and size of human erythrocytes by protein kinases A and C].

The effect of 12-O-tetradecanoyl-phorbol-12-acetate (TPA) and dibutyryl-3,5-cAMP on the shape, volume and protein phosphorylation in human red blood cells (RBC) was studied. TPA (but not cAMP) reduced the average volume of RBC and their transformed definite pool in the cup-shaped form. The changes in the physical parameters were accompanied by an increase in the cytoskeleton protein phosphorylation. An additive effect of cAMP and TPA on the phosphorylation of bands 4.1 and 4.9 was established, thus indicating that distinct domains of amino acid residues were phosphorylated by these stimuli. It was concluded that protein kinase C regulates the shape and volume of human RBC. A model, in which the state of spectrin 4.1-actin and actin 4.9-myosin complexes define the shape and volume of RBC and thus influence ion transport, is proposed.

Bucladesine↗
PubMed1988

[Restriction fragment length polymorphism of c-fos and c-src oncogene loci in spontaneously hypertensive (SHR) and control (WKY) rats].

Interstrain restriction fragments length polymorphism (RFLP) was detected after Southern blot hybridization of DNA from spontaneously hypertensive rats (SHR) and WKY rats treated with Bam HI restrictase with c-fos probe. The SHR genome is characterized by an additional miner band of 4.0 kilobase. RFLP was also revealed in c-src locus by Eco RI and Hind III restrictases. The major characteristic bands are 1.6 kb (SHR) and 2.4 kb (WKY) after Eco RI restriction and 3.4 kb (SHR) and 4.1 kb (WKY) after Hind III restriction. These RFLP can be used as mendelian traits in the linkage studies of distribution of blood pressure and other quantitative physiological traits in (SHR x WKY) F2 hybrids. The interstrain polymorphism determined in c-fos and c-src can also appear important in the evaluation of their physiological role in the cell.

Animals↗
PubMed1988

[Development of the membrane concept of the pathogenesis of primary arterial hypertension].

The membrane concept of primary hypertension involves an alteration of the cation-transport function and the structure of cells' plasmatic membrane. These alterations entail an increase in concentration of cytoplasmatic free calcium followed, in its turn, by an alteration of contractile properties of vascular smooth muscle cells and by a disorder in the mechanisms of neurotransmitter action. A pathogenic association was revealed between the "membrane defect" in primary hypertension and the disturbance in functions of cellular oncogenes (protooncogenes). The association was corroborated both indirectly and by the data on the DNA in the primary hypertension model in the SHR.

Animals↗
PubMed1988

[Characteristics of the structural-functional status of erythrocyte membranes in 3 strains of rats with spontaneous genetic hypertension].

Erythrocyte membrane 22Na and 45Ca transport, osmotic stability and antigenic composition were investigated in 3 strains of rats with spontaneous hereditary hypertension (SHR, SHR SP, MHS), as well as normotensive controls for SHR and SHR SP (WKY) and for MHS (MHS). All strains of spontaneously hypertensive rats showed increased passive membrane permeability for sodium, that was due to increased operation rate of the Na+, K+-cotransport system. Metabolizing sodium is increased in the erythrocytes of Japanese rats (SHR and SHR SP), and decreased in Milan rats (MHS), as compared to normotensive controls. After four hours of incubation with orthovanadate, erythrocyte 45Ca levels were 2-3 times as high in SHR and SHR SP as they were in WKY. In the presence of valinomycin, erythrocyte resistance to hypoosmotic hemolysis was essentially higher in SHR and SHR SP than it was in WKY. These differences are related to a changed rate of anion transport through the band 3 protein. There were no differences in this respect between MHS and MNS. An antigen with a molecular weight of 37-39 kD was detected in erythrocyte membranes of WKY and could not be detected in erythrocytes of other rat groups, including the MNS. It is suggested that different molecular origins of membrane disorders may be an immediate cause of different mechanisms of arterial hypertension in Japanese and Milan animals.

Animals↗
PubMed1988

[Protein kinase A and C activity of erythrocytes in patients with essential hypertension].

Activities of protein kinases A and C in erythrocyte cytoplasmic fraction purified by CM-Sephadex and DEAE-cellulose have been measured. Protein kinase C activity is shown to be 1.6-1.8-fold higher, as compared to controls, in essential hypertension, but remain unchanged in renal hypertension. Protein kinase A activity is slightly elevated in patients with essential hypertension, but the difference is not significant. It is suggested that the increase of protein kinase C activity, and perhaps some other activities as well, in essential hypertension may be a result of altered expression of protooncogenes with protein kinase activities.

Adult↗
PubMed1987

[Membrane defect in primary arterial hypertension: a reflection of dysfunction of cellular oncogenes?].

A hypothesis is proposed, defining the basis of membrane defect associated with primary hypertension as alterations in the cell membrane oncogenes (protooncogenes), whose protein products are represented in the cell plasma membrane as receptors, cytoskeleton and ion transport regulating enzymes (protein kinases, phosphoinositide kinases), growth factors or similar substances. The proposition is based on a group of patterns, characteristic of primary hypertension and absent in its secondary forms, such as: Selective localization of initial alterations in cell plasmatic membranes; Enhanced proliferation of different cell types (vascular smooth muscles, myocardiocytes, blood cells, nerve cells, etc.) which is similar to the manifestation of the effect of tissue growth factors; Activated phosphoinositide metabolism in the cell plasmatic membrane; Imitation of the membrane defect, characteristic of primary hypertension, with the activation of protein kinase C.

Animals↗
PubMed1987

[Genetic analysis of inheritance of Na+, K+-cotransport rate, calcium level in erythrocytes and blood pressure in F2 hybrids of spontaneously hypertensive and normotensive rats].

Positive correlation between Na+, K+-cotransport speed values in platelets and arterial pressure (AP) medium values was disclosed in F2 murine hybrids with spontaneous hypertension (SHT) and in WKY controls as was the correlation between Ca erythrocytic levels and the value of delta AP-AP1-AP2, with AP1--systolic AP measured in alert animals, AP2--medium AP measured directly in anesthetized rats. The data obtained during the aforementioned experimental series together with those obtained in the premorbid stage provided for a conclusion that all the signs considered were inherited in chain with a positive deposit in AP and played an important role in the pathogenesis of primary arterial hypertension.

Animals↗
PubMed1987

[Free calcium concentrations in the nerve endings in the brain of rats with spontaneous hypertension].

Fluorescent indicator Quin-2 was used for the determination of free calcium (Ca2+in) in synaptosomes incubated in the normal medium and media where sodium is replaced by potassium or choline. At external calcium concentration of 1 mM, Ca2+in in all three media was 20-30% higher in synaptosomes of spontaneously hypertensive rats (SHR) than in control animals. At external calcium concentration of 5 mM, the increase in Ca2+in values induced by K+-depolarization in sodium- or choline-containing media was 50-80% higher in synaptosomes of SHR. These differences are suggested to be the basis for the mechanism of increased peripheral chain activity in the sympathetic nervous system in primary hypertension.

Aminoquinolines↗