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Biomedical subjects

Y V Postnov

Publications and source records attributed to Y V Postnov.

At least 37 records · Page 2Linked to original sources
PubMed1988

Transport of sodium and protons and hypotonic haemolysis in the valinomycin-treated erythrocytes of rats with spontaneous hypertension.

After the addition of valinomycin into the incubation medium, the potassium content of rat erythrocytes rapidly decreases. The rate-limiting step of this reaction is a unidirectional efflux of anions through band 3 protein. The rate of this efflux in erythrocytes of spontaneously hypertensive rats (SHR) of the Wistar-Kyoto strain, is not altered. The loss of KCl by rat erythrocytes is accompanied by a decrease in intracellular water, cell shrinking and activation of Na+-H+i exchange. The rate of Na+-H+ exchange in the erythrocytes of SHR in the pre-hypertensive stage (4 weeks old) was decreased by 30%. There were no differences between 14-week-old and 28-week-old SHR and normotensive Wistar-Kyoto (WKY) rats. The half-maximal increase of the valinomycin-induced Na+-H+ exchange in erythrocytes of 14-week-old WKY and SHR was observed at KCl concentrations in the incubation medium of 25 and 40 mmol, respectively. The addition of activators of protein kinase A (dibutyryl-cAMP) or protein kinase C (beta-phorbol ester) resulted in an increase in the maximal rate of Na+-H+ exchange, and did not modify its dependence on K+o concentration. In all groups of SHR, the rate of valinomycin-induced H+ efflux from erythrocytes in the sodium-free medium was 1.5-2.5-fold higher than in age-matched WKY. Under these conditions (addition of valinomycin and inhibition of Na+-H+ exchange), haemoglobin release from erythrocytes of SHR, treated with hypotonic solution, was significantly decreased. We conclude that these differences are due to the alteration of the skeleton protein organization in the erythrocyte membranes of SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Calcium transport in erythrocytes of rats with spontaneous hypertension.

In Quin-2-loaded erythrocytes of two genetically hypertensive rat strains (spontaneously hypertensive rats, SHR, and the Milan hypertensive strain, MHS) intracellular Ca2+ (Ca2+i) concentration and 45Ca influx rate were increased by 25-30 and 15-20% respectively, in comparison with normotensive controls (Wistar-Kyoto rats, WKY, and rats of the Milan normotensive strain, MNS). After 4 h incubation in the presence of 5 mmol/l sodium vanadate (Na3VO4) as an inhibitor of Ca-ATPase, 45Ca content of intact erythrocytes of SHR was twofold higher while erythrocyte count of stroke-prone SHR (SHRSP) was threefold higher than in WKY. This increase was observed in SHR during the pre-hypertensive stage. Under the same conditions, no difference was noted between MHS and MNS rats. The rate of 32P influx, as well as the concentration of exchangeable chloride, was studied. We failed to detect any significant differences in either parameter between hypertensive and normotensive rats, suggesting that altered cell membrane potential was not responsible for allied Ca fluxes. Erythrocyte shrinking, however, resulted in a two to threefold increase in the rate of 45Ca influx. Neither the rate of 45Ca influx nor Ca2+i were modified by the inhibitor of calmodulin-dependent reactions, R24571 (10 mumol/l). It is suggested that the higher rate of Ca2+ influx in Quin-2-loaded erythrocytes of SHR, as well as the increment in 45Ca content in intact erythrocytes treated with orthovanadate, is due to a change in membrane skeleton organization and cell shrinkage.

Aminoquinolines↗
PubMed1988

Interstrain restriction fragment length polymorphism of c-fos and c-src oncogene loci in spontaneously hypertensive and normotensive rats.

Interstrain restriction fragment length polymorphism was detected after Southern blot hybridization of spontaneously hypertensive (SHR) and control (WKY) rat DNA digested by Bam HI restrictase with a v-fos probe. The SHR genome was characterized by an additional minor band of 4.0 kb. Other restriction fragment length polymorphism was revealed in the c-src locus by Eco RI, Hind III and Pst I restrictases. The major characteristic bands were 1.6 kb (SHR) and 2.4 kb (WKY) after Eco RI restriction; 3.4 kb (SHR) and 4.1 kb (WKY) after Hind III restriction and 4.0 kb (SHR) and 4.6 kb (WKY) after Pst I restriction. This restriction fragment length polymorphism can be used as Mendelian traits in linkage studies on the distribution of blood pressure and other quantitative physiological traits in (SHR x WKY)F2 hybrids.

Animals↗
PubMed1986

Investigation of membrane proteins in rat erythrocytes in spontaneous hypertension by means of spin-label technique.

It has been suggested that alterations in cell membrane proteins may play a role in changes of erythrocyte membrane structure and function in hypertension. In order to characterize the structure of membrane proteins of erythrocytes from spontaneously hypertensive rats (SHR) the spin-label technique with a maleimide spin-label was used. A significant difference was observed in the characteristic electron-spin resonance (e.s.r.) spectrum of the label between samples from normotensive rats and SHR. The difference was eliminated and the spectrum significantly changed after treatment of the labelled membrane with EDTA followed by washing out the EDTA extracts, whereas the same treatment with EDTA without the following washing had no effect on the e.s.r. spectrum. It is concluded that the EDTA extracts different substances in the different rat groups. The spin-label technique is a useful method for distinguishing cell membrane properties in SHR and normotensive rats.

Animals↗
PubMed1985

Evidence of lowered plasma membrane potential in different cell types in primary hypertension.

Basal electric potential in the plasma membrane of synaptosomes and platelets as well as the membrane potential in erythrocytes is lower in spontaneously hypertensive rats than in normotensive animals. Similar potential alterations have been found in platelets and erythrocytes of essential hypertensive patients. The reduction of the basal component of the transmembrane potential in synaptosomes and platelets in primary hypertension is partially or entirely compensated by an increase of its electrogenic component as a result of an enhanced activity of Na+K(+)-ATPase. In erythrocytes of patients with renal hypertension and in Cushing's syndrome no alterations of membrane potential are observed.

Adult↗
PubMed1984

Aggregation, membrane potential, and transport in platelets of spontaneously hypertensive rats.

Aggregation, plasma membrane potential, and calcium uptake by platelets of spontaneously hypertensive rats (SHR) were studied. The sensitivity of SHR platelets to the action of ADP and collagen was increased. The addition of Ca-ionophore (A-23187) resulted in aggregation of SHR platelets at a Ca2+ concentration in the incubation medium 20%-30% lower than that required for aggregation of platelets from normotensive rats. The plasma membrane of SHR platelets was found to be partially depolarized (by 8-10 mV) as compared to that of normotensive controls. This difference was apparently due to a higher membrane permeability for Na+. It is suggested that the increase in 45Ca uptake by SHR platelets is related to an increased rate of Ca2+ diffusion along a potential-dependent channel, due to partial depolarization of plasma membrane.

Animals↗
PubMed1984

Microcalorimetry and electrophoresis of the erythrocyte membrane of spontaneously hypertensive rats.

Abnormalities of both structure and function have been described in the erythrocyte membrane of spontaneously hypertensive rats (SHR). In order to elucidate the molecular basis of these abnormalities we have carried out differential scanning microcalorimetry of the erythrocyte membrane and gel electrophoresis of membrane polypeptides. The partial enthalpy of so-called 'C-transition' (at 63 degrees C) was found to be increased. This may be explained by increased content of band 3 protein in SHR erythrocyte membrane.

Animals↗
PubMed1983

On the interrelation between calmodulin and EGTA in the regulation of the affinity to Ca2+ and the maximal activity of the erythrocyte-membrane calcium pump.

1. Calmodulin distribution in rat erythrocytes and the interrelation between calmodulin and EGTA in regulation of the rate of 45Ca accumulation by erythrocyte-membrane inside-out vesicles were studied. 2. The total content of calmodulin in rat erythrocytes is about 24 mumol/l of cells. About 60% of calmodulin is localized in cytoplasm and 40% (10 mumol/l of cells) of calmodulin is loosely bound to membranes; after subsequent washing by hypotonic solution (membranes A) the content of membrane-bound calmodulin decreases up to 0.1 mumol/l of cells. 3. The addition of exogenous calmodulin to membranes A results in increase of the maximal activity of the Ca-pump and does not influence its affinity to Ca2+. Troponin I (30 microM) completely abolishes the calmodulin effect on the Ca-pump activity without significant alterations in its basal activity. 4. The addition of EGTA in the membrane-washing solution results in decrease of the membrane-found pool calmodulin up to 0.01 mumol/l of cells (membranes B). This procedure is accompanied by decrease of the affinity of Ca-pump to Ca2+ and does not influence its maximal rate. 5. The effect of EGTA treatment (membranes B) on the affinity of Ca-pump to Ca is abolished after addition of micromolar concentrations of calmodulin or millimolar concentration of EGTA in the incubation medium. The increase of EGTA concentration in the incubation medium results in decrease of the affinity of Ca-pump to calmodulin. 6. It is assumed that two essentially different pools of calmodulin participate in the regulation of the activity of Ca-pump. (a) The pool of calmodulin which is loosely bound to membrane (this size is dependent on calmodulin concentration in cytoplasm) determines the maximal activity of Ca-pump. The effect of this calmodulin pool is blocked by troponin I. (b) The tightly bound pool of calmodulin which is removed by EGTA treatment determines the affinity of Ca-pump to Ca. 7. In this connection the reasons for contradictory data on estimation of calmodulin effect on the kinetic parameters of plasma membrane Ca-pump are discussed.

Animals↗
PubMed1983

Calmodulin-dependent Ca2+ transport across plasma membranes in primary hypertension.

The rate of calcium transport in the erythrocytes in both forms of primary hypertension [essential hypertension (EH) of humans and spontaneously hypertensive rats (SHR)] and in microsomes of SHR brain were studied. In the erythrocyte membranes subjected to calmodulin depletion by EGTA treatment both the affinity of the Ca-pump for Ca2+ and its maximal activity in primary hypertension did not differ from normotensive controls. The addition of exogenous calmodulin to calmodulin-stripped membranes from erythrocytes of EH or SHR and microsomes of SHR brain resulted in a smaller increase of the Ca-pump activity. It is suggested that the decrease of the rate of calmodulin-dependent calcium transport across the plasma membrane may be a cause for the increased intracellular calcium content found in some tissues in primary hypertension.

Animals↗
PubMed1982

Ca2+ binding and membrane fluidity in essential and renal hypertension.

1. Ca2+ -binding ability and membrane structure of red blood cells of patients with essential and renal hypertension were studied. 2. Ca2+ -binding ability of the erythrocyte membrane of patients with essential hypertension was found to be reduced by 30% compared with that of normotensive controls. 3. The rate of lateral diffusion of pyrene in the erythrocyte membrane of patients with essential hypertension was reduced both in the lipid bilayer and in the region of annular lipid compared with that of normotensive patients. 4. There are no differences either in Ca2+ -binding ability or in fluidity of the erythrocyte membrane of patients with chronic renal hypertension compared with that of normotensive individuals.

Adult↗
PubMed1980

Alteration of intracellular calcium distribution in the adipose tissue of patients with essential hypertension.

The in vitro study of the kinetics of 45Ca efflux from human adipose tissue (omentum major) reveals three pools of exchangeable calcium. The most rapidly exchangeable pool (A) corresponds to extracellular calcium, the two more slowly exchangeable pools (B and C), to intracellular calcium. In the adipose tissue of patients with essential hypertension, the calcium content of the two intracellular pools is increased by 71% and 83%, respectively, as compared to that in normotensive patients.

Adipose Tissue↗
PubMed1980

Evidence of altered calcium accumulation and calcium binding by the membranes of adipocytes in spontaneously hypertensive rats.

Calcium accumulation and calcium binding (ATP--dependent and ATP-independent calcium uptake) by the fragmented plasma membrane, the cytoplasmic reticulum and the mitochondria of isolated adipocytes obtained from spontaneously hypertensive (SHR, Kyoto-Wistar) and normotensive Wistar and Kyoto-Wistar rats were studied by means of isotopic (45Ca) exchange in vitro. The value of ca accumulation in the cytoplasmic reticulum fraction of adipocytes obtained from SHR was found decreased, while in the mitochondrial fraction it was considerably greater as compared to those in both normotensive control groups. Ca binding (ATP independent) by the plasma membrane fraction of hypertensive rats was less than that of the normotensive rats. There was no difference between the groups studied in calcium binding ability for the cytoplasmic reticulum fraction of adipocytes. These results seem to indicate that the adipose cells of hypertensive rats have an alteration of the membrane mechanism maintaining intracellular calcium distribution.

Adipose Tissue↗
PubMed1980

Calcium accumulation and calcium binding by the cell membranes of cardiomyocytes and smooth muscle of aorta in spontaneously hypertensive rats.

1. The ability of isolated membrane fractions of cardiomyocytes, aortic smooth muscle and erythrocytes from spontaneously hypertensive rats to bind calcium was investigated isotopically. 2. Plasma membranes of aortic smooth muscle and erythrocytes of spontaneously hypertensive rats possess a lower calcium-binding ability than preparations from normotensive controls. 3. Sarcoplasmic reticulum from the myocardium of spontaneously hypertensive rats had a lower ability to accumulate calcium. 4. Changes in the calcium-binding ability of the erythrocyte membrane of spontaneously hypertensive rats was related to the diminution of the amount of exchangeable calcium on the inner part of the membrane. The latter may be the cause of the increase of erythrocyte membrane permeability for sodium in spontaneously hypertensive rats and in patients with essential hypertension.

Animals↗