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Biomedical subjects

S N Orlov

Publications and source records attributed to S N Orlov.

At least 19 recordsLinked to original sources
PubMed1992

Sodium-hydrogen exchange in erythrocytes of patients with acute deep venous thromboses.

The rate of delta microH(+)-induced Na/H-exchange in erythrocytes of patients with occlusive and with floating types of acute deep venous thromboses, and in control volunteers, was estimated. In patients with occlusive thrombi Na/H-exchange was revealed to be fourfold higher in comparison with patients with floating thrombi and with controls, while no difference was observed between the two latter groups.

Adult↗
PubMed1992

Volume-dependent regulation of sodium and potassium fluxes in cultured vascular smooth muscle cells: dependence on medium osmolality and regulation by signalling systems.

To identify ion transport systems involved in the maintenance of vascular smooth muscle cell volume the effects of incubation medium osmolality and ion transport inhibitors on the volume and 86Rb and 22Na transport in cultured smooth muscle cells from rat aorta (VSMC) have been studied. A decrease of medium osmolality from 605 to 180 mosm increased intracellular water volume from 0.6 to 1.3 microliters per 10(6) cells. Under isosmotic conditions, cell volume was decreased by ouabain (by 10%, P less than 0.005) but was not influenced by bumetanide, furosemide, EIPA and quinidine. These latter compounds were also ineffective in cell volume regulation under hypotonic buffer conditions. Under hyperosmotic conditions, cell volume was decreased by bumetanide (by approximately 7%, P less than 0.05) and by ethylisopropyl amiloride (by approximately 13%, P less than 0.005). Ouabain-sensitive 86Rb influx was decreased by 30-40% under hypoosmotic conditions. An increase in medium osmolality from 275 to 410 mosm resulted in an approximately eightfold increase in bumetanide-inhibited 86Rb influx and 86Rb efflux. The (ouabain and bumetanide)-insensitive component of 86Rb influx was not dependent on the osmolality of the incubation medium. However (ouabain and bumetanide)-insensitive 86Rb efflux was increased by approximately 1.5-2 fold in VSMC incubated in hypotonic medium. Ethylisopropyl amiloride-inhibited 22Na influx was increased by approximately sixfold following osmotic-shrinkage of VSMC. The data show that both Na+/H+ exchange and Na+/K+/2Cl- cotransport may play a major role in the regulatory volume increase in VSMC. Basal and shrinkage-induced activities of Na+/K+/2Cl- cotransport in VSMC were similarly sensitive to inhibition by either staurosporin, forskolin, R24571 or 2-nitro-4-carboxyphenyl N,N-diphenylcarbomate (NCDC). In contrast basal and shrinkage-induced Na+/K+/2Cl- cotransport were differentially inhibited by NaF (by 30 and 65%, respectively), suggesting an involvement of guanine nucleotide binding proteins in the volume-sensitive activity of this carrier. Neither staurosporin, forskolin, R24571 nor NCDC influenced shrinkage-induced Na+/H+ exchange activity. NaF increased Na+/H+ exchanger activity under both isosmotic and hyperosmotic conditions. These data demonstrate that different intracellular signalling mechanisms are involved in the volume-dependent activation of the Na+/K+/2Cl- cotransporter and the Na+/H+ exchanger.

Alkaloids↗
PubMed1992

Na(+)-K+ pump and Na(+)-K+ co-transport in cultured vascular smooth muscle cells from spontaneously hypertensive and normotensive rats: baseline activity and regulation.

OBJECTIVE: This paper examines the hypothesis that aberrations in vascular smooth muscle univalent ion transport systems play an important role in the pathogenesis of hypertension. DESIGN: Baseline Na(+)-K+ pump and Na(+)-K(+)-2Cl- co-transport activities and the regulation of these ion transport systems by angiotensin II and second messenger molecules have been studied in cultured aortic smooth muscle cells (VSMC) from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). METHODS: Ion transport was studied using isotopic univalent cations (86Rb and 22Na). RESULTS: Baseline Na(+)-K+ pump activity was comparable between SHR- and WKY-derived VSMC. Baseline Na(+)-K(+)-2Cl- and K(+)-Cl- co-transport activity as well as K+ leakage were significantly greater in SHR VSMC. Baseline Na(+)-K(+)-2Cl- co-transport was sensitive to inhibition by forskolin and ethyleneglycol-bis-(beta-amino ethylester)-N,N,N',N'-tetraacetic acid, whereas cyclic guanosine monophosphate and phorbol 12-myristate, 13-acetate had no effect. Angiotensin II-stimulated Na(+)-K(+)-2Cl- co-transport activity did not differ between WKY and SHR VSMC. Angiotensin II increased Na(+)-K(+)-pump activity to a significantly greater extent in SHR VSMC. The stimulatory effect of angiotensin II upon Na(+)-K+ pump activity was reduced under Na(+)-free buffer conditions and in the presence of the Na(+)-H+ exchange inhibitor, ethylisopropyl amiloride. Na(+)-K+ pump activity was also stimulated by the protein kinase C activator, phorbol 12-myristate, 13-acetate, and this was completely inhibited under Na(+)-free buffer conditions. CONCLUSIONS: SHR VSMC exhibit anomalous Na(+)-K(+)-pump and Na(+)-K(+)-2Cl- co-transport activities. The influence of these univalent ion transport systems upon cellular Na+ and Ca2+ homeostasis invoke their participation in the pathogenesis of hypertension.

Angiotensin II↗
PubMed1991

Na+/H+ exchange in erythrocytes of spontaneously hypertensive rats: a study in F2 SHR x WKY hybrids.

The rate of proton gradient-induced Na+/H+ exchange in the erythrocytes of SHR was increased by 50-60% as compared to WKY animals. No significant correlation between Na+/H+ exchange and blood pressure was revealed in F2 hybrids of SHR and WKY rats. Na+/H+ exchange rate in the erythrocytes of F2 SHR x WKY hybrids was twice as high as in SHR and three times higher than in WKY rats.

Amiloride↗
PubMed1991

Ion transport systems in erythrocyte membrane of spontaneously hypertensive rats (SHR) as compared with normotensive rats of the Brown Norway (BN.lx) strain.

The activity of Na+, K(+)-ATPase in SHR erythrocytes treated with saponin is increased by 30-40% as compared to the Brown Norway (BN.lx) strain whereas the activity of Ca(2+)-ATPase is decreased by 20-30%. Passive permeability of SHR erythrocytes determined by 86Rb influx is increased by 20-30%. In the presence of orthovanadate erythrocytes of SHR accumulate 45Ca by 80% more than BN.lx red cells. There was no difference in Na+/H+ exchange between erythrocytes of SHR and BN.lx animals.

Animals↗
PubMed1991

Cation transport and adenosine triphosphatase activity in rat erythrocytes: a comparison of spontaneously hypertensive rats with the normotensive Brown-Norway strain.

The activity of transport adenosine triphosphatases (ATPases) in saponin-treated erythrocytes as well as the passive membrane permeability for 86Rb+ (K+), 45Ca2+ uptake (in the presence of orthovanadate) and the rate of Na(+)-H+ exchange in intact erythrocytes were studied in spontaneously hypertensive rats (SHR), Wistar-Kyoto (WKY) and Brown-Norway (BN.lx) rats. Higher Na+,K(+)-ATPase activity, lower Ca(2+)-ATPase activity, increased passive K+ permeability and greater 45Ca2+ uptake were observed in erythrocytes from SHR compared with BN.lx rats. Similar differences in the last two parameters were also disclosed by a comparison of SHR and WKY rats. The rate of Na(+)-H+ exchange in SHR erythrocytes was greater than in WKY rats but equal to that of BN.lx rats. A genetic analysis did not reveal a significant correlation between Na(+)-H+ exchange rate and blood pressure in F2 SHR x WKY hybrids.

Adenosine Triphosphatases↗
PubMed1991

On the mechanism of shrinkage-induced potassium influx in rat and human erythrocytes.

The rates of 86Rb influx into human and rat erythrocytes were studied in media of various tonicity. At sucrose concentrations below 0.3 mol/l, the ouabain-insensitive, furosemide-inhibited component of influx increased in rat but not in human erythrocytes; this may be explained by a rise in the rate of Na+, K+, Cl-- and/or K+, Cl-cotransport. An increase in osmolarity resulted in a reduction of this as well as of the ouabain and furosemide-insensitive component in rat erythrocytes. At the same conditions a drastic inhibition of Na+, K(+)-pump occurred both in rat and human erythrocytes. We failed to observe a lag-phase in the activation of the cotransport in rat erythrocytes; i. e. the process of activation parallels the shrinkage of cells. In rat erythrocyte ghosts, the shrinkage-induced stimulation of the cotransport was lost, and the direction of their osmotic reaction (inhibition of transport pathways) was similar to that in human erythrocyte ghosts. It is suggested that the mechanism of volume regulation of ion transport in intact cells involves a step of physical amplification via a change in interactions between the protein carcass and the lipid bilayer.

Animals↗
PubMed1991

[The mechanisms of ion transport activation with a change in cell volume].

The review deals with literature and our own experimental data on the possible mechanisms of activation of the ion transport in cells during the change of their volume. The involvement in this process of calcium, cyclic mononucleotides, metabolites of polyphosphoinositides and arachidonic acid, as well as the membrane carcass and cytoskeleton are discussed.

Animals↗
PubMed1991

[Erythrocyte Na+/Li+ countertransport and arterial hypertension: data of a cross-sectional population study].

The relation of red blood cell Na+/Li+ countertransport rate to the prevalence of arterial hypertension (AH) and blood pressure was evaluated in 720 individuals aged 23-60 years. In all age groups, the rate of red blood cell Na+/Li+ countertransport was significantly higher in males than in females. Age, alcohol use, obesity in males and age, obesity, and Na+/Li+ countertransport rate in females are factors that predispose to AH, as evidenced by multivariate logistic analysis. The latter parameter is associated with obesity and diastolic blood pressure and unassociated with age, alcohol use, and smoke, as suggested by regression analysis. The distribution of Na+/Li+ countertransport rate values in the population after standardization for ruling out the impact of obesity is erroneous and shifted to the right. This allows it to be presented as a sum of two normal distributions. However, their analysis has failed to reveal statistically significant differences in blood pressure values of AH incidence. The rate of Na+/Li+ countertransport may be regarded as a biological population risk factor for AH, which is, however, less than such factors as age, obesity, and excessive alcohol use.

Adult↗
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↗