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Biomedical subjects

S N Orlov

Publications and source records attributed to S N Orlov.

At least 91 records · Page 5Linked to original sources
PubMed1991

[The role of the rate of sodium-lithium countertransport of the erythrocytes in arterial hypertension].

The present work is concerned with the role of the velocity of Na+/Li(+)-countertransport of red blood cells (as an indicator of the function of cellular membranes) in the development of arterial hypertension under conditions of a populational study. A relationship is demonstrated between the velocity of Na+/Li(+)-countertransport and the sex, arterial pressure, body mass index, and blood serum triglycerides. The high velocity of Na+/Li(+)-countertransport is encountered in 25% of the population, being responsible for about 30% of all cases of arterial hypertension. Taking into consideration the modern multifactorial theory of the genesis of arterial hypertension, the high velocity of Na+/Li(+)-countertransport should be viewed as a definite disease pattern (one of several) and as a risk factor of arterial hypertension in women (the data of the prospective part of the study).

Adult↗
PubMed1991

[The transport of monovalent ions and calcium in the erythrocytes of patients with bronchial asthma].

The intracellular levels of sodium, potassium, and free calcium, as well as red blood cell transport of 86Rb (a radioactive potassium analogue) and 45Ca were measured in patients with bronchial asthma (BA). The intracellular content of sodium was 10-20% higher in patients with BA, though the differences in the present sample (7 controls and 18 BA patients) failed to be significant (p less than 0.05). The differences were most pronounced in infection-dependent BA and not eliminated during glucocorticoid hormone therapy. The activity of the Na+, K+ pump, as assessed by the values of an ouabain-inhibited component of 86Rb entry, was increased by 10-20% (p less than 0.05) in BA patients and of Na+, K+ cotransport (an ouabain-sensitive furosemide-inhibited component of 86Rb entry), by 35-45% (p less than 0.25). The passive red blood cell membrane permeability in BA patients (an ouabain + furosemide-insensitive component of 86Rb) remained unchanged. The quin-2-loaded red blood cell entry rate for 45Ca was decreased by 5-10%. In the absence of a Ca(2+)-ATPase inhibitor (0.5 mM orthovanadate), these differences were greatly significant (p less than 0.005). In addition, the patients with BA showed a 10% reduction in free calcium levels; however, the differences were insignificant (p less than 0.25), which might be caused by Ca-pump activation. As in the experiments with Na+ level measurements, the greatest differences in red blood cell Ca(2+)-balance control were recorded in patients with infection-dependent BA and independent of glucocorticoid hormone therapy. Possible mechanisms of involvement of the changes found in monovalent cation and Ca2+ transport in the pathogenesis of BA were also discussed.

Adult↗
PubMed1991

[Peptide hydra morphogen activates Na/H-exchange in human erythrocytes].

The effect of peptide morphogen of hydra (PMH) on Na+/H+ exchange in human erythrocytes was studied. It was shown that this peptide leads to 2-7 fold activation of the rate of protons efflux from the human erythrocytes at concentration 100 nM. It was assumed, that peptide controls and regulates proliferation via the activation Na+/H+ exchange.

Amiloride↗
PubMed1991

[Erythrocyte sodium-lithium countertransporter level as a risk factor of hypertension (prospective study data)].

A 3-year prospective study was undertaken to evaluate the relation of red blood cell Na+/Li+ countertransport rates to the incidence of arterial hypertension. A total of 227 subjects (males and females aged 24-54 years)--a 20% representative sample of organized population--was followed up. The annual incidence of arterial hypertension was 4.3 among males and 2.7 among females. The baseline blood pressures and obesity in males and rates of Na+/Li+ countertransport in females were demonstrated to be factors associated with the incidence of arterial hypertension. The rate of red blood cell Na+/Li+ countertransport can be regarded as an independent biological risk factor for arterial hypertension.

Adult↗
PubMed1990

The ATPase activity of saponin-treated rat erythrocytes: regulation by monovalent cations, calcium, ouabain, and furosemide.

The ATPase activities were studied in rat erythrocytes permeabilized with saponin. The concentrations of calcium and magnesium ions were varied within the range of 0.1-60 microM and 50-370 microM, respectively, by using EGTA-citrate buffer. The maximal activity of Ca2(+)-ATPase of permeabilized erythrocytes was by one order of magnitude higher, whereas the Ca2(+)-binding affinity was 1.5-2 times higher than that in erythrocyte ghosts washed an isotonic solution containing EGTA. Addition of the hemolysate restored the kinetic parameters of ghost Ca2(+)-ATPase practically completely, whereas in the presence of exogenous calmodulin only part of Ca2(+)-ATPase activity was recovered. Neither calmodulin nor R24571, a highly potent specific inhibitor of calmodulin-dependent reactions, influenced the Ca2(+)-ATPase activity of permeabilized erythrocytes. At Ca2+ concentrations below 0.7 microM, ouabain (0.5-1 mM) activated whereas at higher Ca2+ concentrations it inhibited the Ca2(+)-ATPase activity. Taking this observation into account the Na+/K(+)-ATPase was determined as the difference of between the ATPase activities in the presence of Na+ and K+ and in the presence of K+ alone. At physiological concentration of Mg2+ (370 microM), the addition of 0.3-1 microM Ca2+ increased Na+/K(+)-ATPase activity by 1.5-3-fold. Higher concentrations of this cation inhibited the enzyme. At low Mg2+ concentration (e.g., 50 microM) only Na+/K(+)-ATPase inhibition by Ca2+ was seen. It was found that at [NaCl] less than 20 mM furosemide was increased ouabain-inhibited component of ATPase in Ca2(+)-free media. This activating effect of furosemide was enhanced with a diminution of [Na+] upto 2 mM and did not reach the saturation level unless the 2 mM of drug was used. The activating effect of furosemide on Na+/K(+)-ATPase activity confirmed by experiments in which the ouabain-inhibited component was measured by the 86Rb+ influx into intact erythrocytes.

Adenosine Triphosphatases↗
PubMed1990

[Characteristics of adenosine triphosphatase activity in carp erythrocytes treated with saponin].

The activities of Ca-ATPase and Na,K-ATPase in saponin-treated erythrocytes of man, rat and carp were compared. It was shown that at free calcium concentrations lower than 1 microM the activity of Ca-ATPase in carp erythrocytes was by one order of magnitude lower than in rat erythrocytes and 3-4 times lower than in human red blood cells. At [Ca2+] = 0.4 microM the activities of Na,K-ATPase in all species under study were essentially the same. The increase in Ca2+ concentration up to 1 microM resulted in a 2-5-fold activation of Na,K-ATPase in rat and carp erythrocytes, respectively. In all cases studied a further elevation of free calcium concentration was accompanied by a decline of the Na,K-ATPase activity. It was shown that the Pi content in carp erythrocytes is 5-6 times as high as that in mammalian cells. This circumstance is a considerable obstacle to a detailed analysis of mechanisms of ATPase activity regulation in carp erythrocytes by methods used for determination of inorganic phosphate production.

Animals↗
PubMed1990

Volume-dependent regulation of cation transport and polyphosphoinositide metabolism in human and rat erythrocytes: features revealed in primary hypertension.

The rate of delta mu H+ --induced erythrocyte Na+/H+ exchange is increased in both patients with essential hypertension (EH) and spontaneously hypertensive rats (SHR). The increase of Na+,K(+)-cotransport was revealed in erythrocytes of SHR only. This alteration as well as a decrease of mean cell volume were observed in both young and old erythrocytes of SHR. The moderate shrinkage of rat (but not human) erythrocytes results in an increase of the rate of Na+,K(+)-cotransport. The more pronounced shrinkage of rat (but not human) erythrocytes induces the Na+/H+ exchange. These reactions are accompanied by phosphoinositide response. Activator of protein kinase C (TPA) increases delta mu H+ --induced Na+/H+ exchange both in human and rat erythrocytes but it does not modify phosphoinositide metabolism. No differences were observed in the rate of Na+/H+ exchange between TPA-treated erythrocytes of SHR and WKY. We assume that the activation of protein kinase C increases Na+/H+ exchange in primary hypertension. Increased Na+/H(+)-cotransport revealed in an experimental model of primary hypertension is probably due to the decrease of erythrocyte volume.

Adult↗
PubMed1990

Protein kinase C activity in erythrocytes in primary hypertension: regulation of cell shape and cation transport.

Protein kinase C activity in the lysate of erythrocytes of patients with essential hypertension (EH) and spontaneously hypertensive rats (SHR) was found to be increased by 1.6-2.0 times as compared with normotensive controls. Membrane cytoskeleton alterations observed in the erythrocytes of patients with EH and SHR were revealed in decreased average erythrocyte volume, increase of cup-shaped cell formation, and increase of basal phosphorylation of band 4.9 protein. In addition, the rate of Na(+)-H+ exchange in erythrocytes of EH patients and SHR was increased by 1.9-fold. In vitro treatment of erythrocytes of healthy donors and Wistar-Kyoto rats (WKY) with protein kinase C activator (12-O-tetradecanoylphorbol-13-acetate) leads to similar changes of cell shape, cell volume, band 4.9 protein phosphorylation and Na(+)-H+ exchange, as well as to an increase of diS-C3-(5) fluorescence. It may be assumed that alterations of these parameters revealed in primary hypertension are caused by increased activity of protein kinase C.

Adult↗
PubMed1990

Thermal inactivation of membrane proteins, volume-dependent Na+, K(+)-cotransport, and protein kinase C activator-induced changes of the shape of human and rat erythrocytes.

The heat sorption curves for human and rat erythrocyte membranes in the temperature region from 40 degrees C to 90 degrees C have been compared resulting from thermal gel analysis of these membranes. The main heat sorption peaks are located within the temperature regions from 49 degrees C to 52 degrees C (A transition), from 56 degrees C to 59 degrees C (B transition), from 62 degrees C to 65 degrees C (C transition) and from 74 degrees C to 82 degrees C (D transition). Thermoinactivation temperatures for most of the membrane proteins in human and rat erythrocytes are rather different, which suggests essential differences in the arrangement of their membrane frameworks. Addition of the protein kinase C activator TPA induces a fast increase in light scattering of human and rat erythrocyte suspension which is connected with some changes of cell shape. This reaction is completely blocked by a minimal thermal treatment of the membrane framework proteins (preincubation at the temperature of the A transition). Such treatment inhibits also the increase of Na+, K(+)-cotransport in rat erythrocytes induced by hyperosmotic shrinkage. It is assumed that the proteins of the membrane framework take part in the volume-dependent regulation of the ion-transport systems of plasma membranes.

Animals↗
PubMed1989

Volume-dependent regulation of ion transport and membrane phosphorylation in human and rat erythrocytes.

Osmotic swelling of human and rat erythrocytes does not induce regulatory volume decrease. Regulatory volume increase was observed in shrunken erythrocytes of rats only. This reaction was blocked by the inhibitors of Na+/H+ exchange. Cytoplasmic acidification in erythrocytes of both species increases the amiloride-inhibited component of 22Na influx by five- to eight-fold. Both the osmotic and isosmotic shrinkage of rat erythrocytes results in the 10- to 30-fold increase of amiloride-inhibited 22Na influx and a two-fold increase of furosemide-inhibited 86Rb influx. We failed to indicate any significant changes of these ion transport systems in shrunken human erythrocytes. The shrinking of quin 2-loaded human and rat erythrocytes results in the two- to threefold increase of the rate of 45Ca influx, which is completely blocked by amiloride. The dependence of volume-induced 22Na influx in rat erythrocytes and 45Ca influx in human erythrocytes on amiloride concentration does not differ. The rate of 45Ca influx in resealed ghosts was reduced by one order of magnitude when intravesicular potassium and sodium were replaced by choline. It is assumed that the erythrocyte shrinkage increases the rate of a nonselective Cao2+/(Nai+, Ki+) exchange. Erythrocyte shrinking does not induce significant phosphorylation of membrane protein but increases the 32P incorporation in diphosphoinositides. The effect of shrinkage on the 32P labeling of phosphoinositides is diminished after addition of amiloride. It is assumed that volume-induced phosphoinositide response plays an essential role in the mechanism of the activation of transmembrane ion movements.

Amiloride↗
PubMed1989

Interstrain restriction fragment length polymorphism in the c-src correlates with Na,K cotransport and calcium content in hybrid rat erythrocytes.

Twenty-six F2 hybrids between spontaneously hypertensive (SHR) and normotensive control (WKY) rats [(SHR x WKY)F2] were segregated according to their c-src genotype into SS and WW homozygous groups, corresponding to SHR or WKY and a WS heterozygous group. The Na,K cotransport in erythrocytes in the WW group was equal to that of WKY and differed significantly from that of the WS and SS groups (the rate of Na,K cotransport in the latter groups was close to that of the SHR). The calcium content of the erythrocytes in the WW group was equal to that of the WKY, but lower than that of the WS and SS groups which, in turn, was significantly lower than that in the SHR, indicating polygenic control of the trait. We concluded that the c-src locus itself or some other loci inherited in conjunction with the c-src determines the increase in Na,K cotransport and in calcium content in erythrocytes of SHR.

Animals↗
PubMed1989

Na+-H+ exchange and other ion-transport systems in erythrocytes of essential hypertensives and spontaneously hypertensive rats: a comparative analysis.

The activity of ion-transport systems and Ca2+-induced erythrocyte haemolysis were compared between patients with essential hypertension and two strains of spontaneously hypertensive rats. Previous data on the increased rate of Na+-Li+ countertransport in erythrocytes of essential hypertensives were confirmed in this study. However, identification of Na+-Li+ countertransport in rat erythrocytes remained a complicated person because of the high rate of sodium-independent efflux of Li+. The rate of Na+-H+ exchange increased by 50-80% both in spontaneously hypertensive Wistar-Kyoto rats (SHR) and in patients with essential hypertension. No difference between Milan hypertensive strain rats (MHS) and Milan normotensive strain rats (MNS) was found. The rate of Na+,K+ cotransport increased in SHR and MHS erythrocytes compared with rats of the control strains [normotensive Wistar-Kyoto rats (WKY) and MNS; 30-50 and 90-110%, respectively]. No difference in this parameter was found between patients with essential hypertension and healthy subjects. Erythrocytes of patients with essential hypertension and of SHR were characterized by a higher sensitivity of their K+ channels to the increased concentration of intracellular Ca2+. This parameter did not change in MHS erythrocytes. Ca2+-induced haemolysis increased four- to fivefold in MHS erythrocytes compared with MNS and did not change in erythrocytes of SHR and patients with essential hypertension. The conclusion from these data is that the SHR strain is a more adequate model of human essential hypertension than the MHS.

Adenosine Triphosphatases↗
PubMed1989

Light-dependent Na(+)-Ca2+ exchange in retinal rod discs.

Experiments are described demonstrating that Na(+)-Ca2+ exchange of retinal rod disc membrane is highly sensitive to light. The Na(+)-Ca2+ exchanger was shown to possess two types of binding sites with different affinities for calcium. The low affinity binding sites (KCaD = 5.8 mumol/l) are light-insensitive. After bleaching, KD of the high affinity Ca2(+)-binding sites an Ki for Na+ changed from 0.2 to 0.3 mumol/l and from 3.2 to 0.7 nmol/l, respectively. Light inhibits the steady-state Ca2+ uptake by a factor of 1.5. Photocontrol of the Na(+)-Ca2+ exchanger affinity is observed at the physiological level of rhodopsin bleaching.

Animals↗