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Biomedical subjects

Iu V Postnov

Publications and source records attributed to Iu V Postnov.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1987

[Erythrocyte membrane phosphorylation in rats with spontaneous hypertension as affected by protein kinase C activator].

A study of orthophosphate incorporation into erythrocyte membrane proteins and lipids of spontaneously-hypertensive rats (SHR) at incubation of erythrocytes with 32PO4 and that of erythrocyte ghosts with 32P-gamma-ATP showed basal phosphorylation of proteins as well as polyphosphoinositides of erythrocyte ghosts to be essentially increased in SHRs as compared to normotensive animals, the differences being eliminated by the addition of protein kinase C activator (4 beta-phorbol-12 beta-myristate-13 alpha-acetate, PMA). After PMA-stimulated protein phosphorylation most of the label was incorporated into proteins of Band 4.1. There was no difference in basal phosphorylation of membrane proteins in case of intact erythrocytes. Under PMA stimulation, most of the label was incorporated into proteins of band 4.1 similarly to labelling of erythrocyte ghosts and a significant increment of radioactivity could only be seen in the control animals.

Animals↗
PubMed1987

[Characteristics of Na+/H+ metabolism in the erythrocytes of rats with spontaneous hypertension].

The dependence of the rate of valinomycin-induced Na+/H+ erythrocyte metabolism on the extracellular K+ concentration has been investigated. It has been established that Na+/H+ metabolism in the erythrocytes of spontaneously hypertensive rats (SHR) is induced at higher [K+]o concentrations than in normotensive controls (WKY). The distinctions in the maximum rate of Na+/H+ metabolism were revealed only in SHR in pre-hypertensive stage (it was 20% lower than in WKY). It is suggested that the distinctions are determined by peculiarities of membrane cytoskeleton formation. The conclusion was confirmed in experiments on erythrocyte stability to orthovanadate effect.

Amiloride↗
PubMed1987

[Changes in erythrocyte volume in relation to characteristics of protein phosphorylation of the membrane cytoskeleton in hypertension: role of protein kinase C].

Shape, volume and protein phosphorylation of RBC were studied in normal subjects and patients with essential hypertension. Mean volume of RBC of hypertensive patients was reduced by 3-4%, as compared to the control group. The level of band 4.9 phosphorylation was simultaneously increased in RBC of hypertensive patients. Activation of protein kinase C with phorbol ester produced volume reduction and shape changes in RBC. These changes are accompanied with phosphorylation of bands 4.1 and 4.9. It is suggested that RBC volume reduction in essential hypertension may be related to an alteration in the regulation of cytoskeleton proteins phosphorylation.

Enzyme Activation↗
PubMed1986

[The Ca pump and Ca ATPase in the erythrocytes of patients with hypertension: disorders detected in cytoskeletal membranes and in solubilized Ca ATPase].

A study of Ca-ATPase and Ca-pump activity of the erythrocyte membrane's inverted vesicles with different cytoskeletal protein status demonstrated that Ca-pump activity remained unchanged, and Ca-ATPase activity was increased by 20-40%, as compared to erythrocytes from the normotensive controls, in hypertensive patients in the absence of exogenous calmodulin. These differences are assumed to be due to disorders of erythrocyte membrane structure in primary hypertension resulting in less efficient Ca-pump operation in the inverted vesicles. In all types of membranes obtained from hypertensive patients' erythrocytes in conditions of iso-osmotic hemolysis, calmodulin-induced increment of peak Ca-ATPase and Ca-pump activity was 2 or 3 times as low as that of normotensive controls. These differences remained in evidence after the solubilization of membrane proteins with triton X-100. No differences in calmodulin influence on Ca-ATPase affinity to Ca2+ could be found. The membranes obtained in iso-osmotic conditions demonstrated no calmodulin effect on Ca-ATPase activity which is attributed to partial proteolysis of the enzyme's molecule.

Adult↗
PubMed1986

[Electric potential of the erythrocyte membrane in essential hypertension and symptomatic hypertensions].

Electric potential was studied in erythrocytes of patients with essential (20) and renal (16) hypertension and in those with the Icenko-Cushing disease (9 patients) by means of fluorescent dye diS-D3-(5). A decrease of membrane potential was found in erythrocytes of essentially hypertensive patients as compared to the normotensive controls (27). No differences were demonstrated in the values of membrane potential between normotensive individuals and patients with secondary hypertension.

Adult↗
PubMed1986

[Dependence of the number of vesicles in vascular smooth muscle cells on the presence of noradrenaline in the extracellular space].

Noradrenaline (NA) effect on the number of vesicles in smooth muscle cells was investigated in small mesenteric arteries of spontaneously hypertensive rats (SHR), aged 8 or 12 weeks, and age-matched normotensive Wistar-Kyoto (WKY) rats. The presence of NA in the incubation medium resulted in an increase in the number of vesicles in SHR of both age groups, but not in WKY. The results are discussed in view of the relationship between the vesicles and Ca transport in smooth muscle cells.

Animals↗
PubMed1986

[Morphology of adrenergic and cholinergic innervation of the kidney as affected by spontaneous and ischemic renal hypertension in rats].

The innervation of basic renal structures (vascular glomerular pole with juxtaglomerular apparatus and renal tubules) was experimentally studied in rats at different stages of spontaneous and Goldblatt hypertension. Both fluorescent determination of adrenergic innervation and histochemical identification of cholinergic innervation have shown that they increased in spontaneous and remained unchanged in renal hypertension. The data obtained confirm an important role of intrarenal innervation in the development of kidney "resettings" in spontaneous hypertension.

Adrenergic Fibers↗
PubMed1986

[Calcium transport in erythrocytes loaded with a highly selective Ca2+ chelator. The characteristics associated with primary hypertension].

The kinetics of 45Ca accumulation was studied in erythrocytes loaded with highly-selective Ca2+ chelator quin-2. Ca2+ erythrocyte penetration rate was increased by 20-30%, and free intracellular calcium (Ca2+ in), by 40-50%, in hypertensive patients, as compared to normotensive controls. Spontaneously hypertensive rats showed no differences in this respect. The addition of valinomycin and quinidine produced a tenfold increase in Ca2+ penetration rate in human erythrocytes and a 1.5-2-fold increase in rat erythrocytes. Under these conditions, the erythrocyte Ca2+ penetration rate and Ca2+ in concentration were increased by 40 and 60%, respectively, in spontaneously hypertensive rats. Hypertensive patients showed no differences. After incubation with the Ca-ATPase inhibitor orthovanadate, erythrocyte calcium level in the absence of quin-2 was 2-3 times as high in spontaneously hypertensive rats as it was in control animals.

Adult↗
PubMed1985

[The membrane theory of primary arterial hypertension (development of the concept of the nature of hypertension)].

The author reviews the data from the recent researches developing the idea which consider primary hypertension as a consequence of wide-spread cell membrane alteration (the membrane conception of primary hypertension). The main recent advances, in favour of this point of view, are the following: demonstration of alteration in the calmodulin-membrane Ca pump interaction in erythrocytes and platelets in human essential hypertension as well as in spontaneous hypertension in rats; registration of lowered plasma membrane electric potential in different types of cells; demonstration of an increased concentration of ionized cytoplasmic calcium in different types of cells. Formation of increased concentrations of free calcium in cell cytoplasm is considered to be the principal pathogenic factor of primary hypertension. Chronic neuropsychic overstrain accelerates the development of hypertension, thus promoting the development of insufficient membrane regulation of cytoplasmic free calcium concentration. At this aspect the membrane conception coincides with the neurogenic theory of essential hypertension by G. Lang.

Animals↗
PubMed1985

[Membrane potential and transport of neuromediators in synaptosomes of the brain of rats with spontaneous hypertension].

The transport of 3H-GABA, 14C-choline, 14C-noradrenaline and 3H-serotonin in brain synaptosomes of spontaneously-hypertensive rats (SHR) which is controlled by the carrier whose activity is dependent on the sodium gradient and electric potential of the plasma membrane was studied. The initial rate of GABA uptake by SHR synaptosomes was reduced by 25%. The steady state of the content of GABA, noradrenaline and serotonin in SHR synaptosomes was reduced by 15-20%, whereas the steady state of choline content by 35%. The differences are levelled when synaptosomes are depolarized, both due to the elimination of K+-diffusion potential, and the opening of Na channels. An increase in the extracellular calcium concentration up to 1 mmol results in a 20% synaptosomal GABA rise that is unrelated to membrane hyperpolarization. In the presence of the Ca-ionophore A-23187, a similar effect is observed with a 1-2 mmol Ca2+ concentration. The electric potential of SHR synaptosomes which is studied by means of the fluorescent dye dis-C3-(5) was shown to be reduced by 5-10 mV. Partial depolarization of SHR synaptosomes is supposed to be the principal cause of the decrease in both the initial rate of uptake and the steady state of the content of neuromediators.

Acetylcholine↗