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Biomedical subjects

S N Orlov

Publications and source records attributed to S N Orlov.

At least 163 records · Page 9Linked to original sources
PubMed1983

[Various characteristics of erythrocyte membrane proteins in rats with spontaneous hypertension].

Differential scanning microcalorimetry demonstrated an increase in specific heat capacity of erythrocyte membranes of spontaneously-hypertensive rats around 63 degrees C (C-transition). Disc electrophoresis with sodium dodecyl sulphate showed the percentage of band 3 peptides to be increased in relation to all membrane peptides in these membranes. It is suggested that the elevated content of band 3 peptides, which are known to participate in the formation of anion channels in mammalian erythrocyte membranes, may be one of the causes of increased specific heat of C-transition.

Animals↗
PubMed1983

[Sodium transport in the erythrocytes of patients with essential and symptomatic (renal) hypertension].

Sodium transport was investigated, using the isotope exchange method, in the erythrocyte membranes of normal subjects and patients with essential and symptomatic (renal) hypertension. In hypertensive patients, the constant of balanced Na/Na exchange rate was increased by more than 60%, and the balance concentration of erythrocytic sodium by 30%, as compared to the controls, in the presence of ouabain. These differences become far less pronounced if furosemide is added to the incubation medium. In patients with secondary (renal) hypertension, the Na/Na exchange rate and erythrocytic balance concentration of sodium are not affected by ouabain as compared to the controls. It is suggested that Na/Na-countertransport plays the principal role in the disruption of erythrocyte membrane permeability by sodium in essential hypertension.

Adult↗
PubMed1982

Evidence of altered structure of the erythrocyte membrane in spontaneously hypertensive rats.

1. The membrane structure of erythrocytes of rats with different forms of arterial hypertension was studied by means of two hydrophobic fluorescent probes (diphenylhexatriene and pyrene). 2. Microviscosity of hydrophobic areas of erythrocyte membrane of spontaneously hypertensive rats was found to be increased compared with that of membranes from normotensive control rats. 3. No alterations of membrane structure of erythrocytes of deoxycorticosterone-treated rats and renal hypertensive rats were found.

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↗
PubMed1982

[Transport of calcium to synaptosomes and subcellular membrane fractions of the brain: effects of opioid peptides].

Highly purified synaptosomal and subcellular fractions identified as mitochondria and microsomes were obtained by fractionation of brain tissues. The greatest Ca-accumulating capacity and the highest rate of Ca2+ accumulation were revealed in the mitochondrial fraction. Upon further fractionation of the synaptosomal fraction the energy-dependent uptake (accumulation) of Ca2+ was revealed only in the mitochondria. It was demonstrated that opioid peptides accelerate Ca2+ uptake by the synaptosomes in a medium with physiological concentration of K+ and inhibit this process during K+-dependent membrane depolarization. It was shown that beta-endorphine, methionine-encephaline and leucine-encephaline (10(-8)-10(-5) M) inhibit the Ca-accumulating capacity of both mitochondria and microsomes from brain. The experimental data suggest that opioid peptides can modulate the release of neurotransmitters and/or neurohormones by inhibiting the potential-dependent Ca2+ influx into the nerve endings and by decreasing the intrasynaptosomal pool of Ca2+.

Animals↗
PubMed1982

[Ca-binding capacity and the membrane structure of the erythrocytes in certain types of experimental hypertension in rats].

The authors studied the microstructure of erythrocyte membrane (using polarization method of fluorescent probes) and its Ca-binding property in rats with spontaneous, renal and DOCA-salt hypertension. Rats with spontaneous hypertension showed increased microviscosity of erythrocyte membrane and decrease in its property of binding Ca ions, which is not recorded in renal and DOCA-salt hypertension. Salt overload exerted no influence on both parameters studied.

Animals↗
PubMed1982

[Effect of monovalent cations on calcium transport in the mitochondria].

Radioisotope exchange was used to study the effect of the Na+/K+ ratio on Ca2+ absorption and release from mitochondria of the rat myocardium, brain and fatty tissue. The increase in Na+ concentration in the incubation medium containing ATP and succinate leads to a 8-fold reduction of the Ca-accumulating capacity of brain mitochondria (K0,5 for Na+ 7 and 30 mM, respectively). A mechanism is suggested that explains the possibility of the Na-dependent regulation of the Ca-accumulating capacity of mitochondria of the tissues under consideration.

Animals↗
PubMed1982

[Calcium transport in the erythrocytes of rats with spontaneous hypertension: characteristics of the effect of calmodulin].

Transport features of calcium in red cells of rats with spontaneous genetic hypertension (SHR) have been studied. It is shown that in the presence of calmodulin the rate of calcium accumulation by the inside-out vesicles of SHR red cell membranes is roughly twice less than in the control normotensive rats. It is suggested that upset interrelationship between calmodulin and Mg-Ca-ATPase of plasma membrane may be the cause of increase of intracellular calcium recorded in a number of tissues in primary hypertension.

Animals↗
PubMed1982

[Characteristics of calcium and sodium transport in the synaptosomes and subsynaptosomal structures of the brain of spontaneously hypertensive rats].

Calcium and sodium synaptosomal uptake and mitochondrial and microsomal accumulation were examined in the brain of rats with inherited spontaneous hypertension, using 45Ca and 22Na labels. In the brain synaptosomes of hypertensive rats and control animals, calcium only arrives via potential-dependent Ca-channels when synaptolemma is depolarized. Basic calcium uptake by brain synaptosomes of hypertensive rats is increased as compared to that of the control animals. Partial depolarization of the synaptosomal plasma membrane in hypertension may be caused by its increased permeability by sodium. When Ca2+ concentrations are low, its mitochondrial accumulation rate is increased, and microsomal rate, on the contrary, decreased in the brain of hypertensive rats. The effect of calmodulin on the microsomal calcium accumulation rate is essentially lower in hypertensive rats as compared to the controls. The described disorders of synaptosomal Ca-transporting systems in rats with spontaneous hypertension can obviously result in changed neuromediator secretion rates in nerve endings.

Animals↗
PubMed1982

[Transport of calcium and distribution of calmodulin in the erythrocytes in primary arterial hypertension].

Calcium transport to inside-out vesicles and calmodulin erythrocytic distribution were examined in primary hypertension, using the isotope exchange method and phosphodiesterase activity measurement. No differences in total erythrocyte calmodulin content and its cytoplasmic and membrane concentrations were detected in either hypertensive patients, or rats with spontaneous hypertension. Differences in the rates of calcium transport through EGTA-treated membranes were only detectable in the presence of exogenous calmodulin. The erythrocytes of hypertensive patients showed a four-fold reduction in the maximum calcium transport rate increment under the effect of calmodulin, as compared to normotensive subjects. These differences are attributed to a possible disruption of calmodulin interaction with Mg, Ca-ATPase.

Adult↗
PubMed1981

Alteration of the intracellular calcium pool of adipose tissue in spontaneously hypertensive rats. No effect of peripheral immunosympathectomy.

The intracellular calcium pool of adipose tissue was estimated by studying the kinetics of 45Ca efflux from the tissue of 9-week old spontaneously hypertensive (SHR) and normotensive Kyoto-Wistar (NKWR) rats subjected to peripheral immunosympathectomy (nerve growth factor antiserum treatment of newborn rats) and in intact (sham-treated) animals of both strains. The development of hypertension in SHR was prevented by immunosympathectomy, however, both groups, SHR-intact and immunosympathectomized rats showed an increase in the intracellular calcium content of adipocytes. These results indicate that the alteration of the membrane control over intracellular calcium distribution in adipose tissue of SHR cannot be attributed to an enhanced activity of the sympathetic nervous system.

Adipose Tissue↗
PubMed1981

[Erythrocyte membrane permeability of sodium in different types of chronic experimental hypertension].

The permeability of the red blood cell membrane for sodium in rats with spontaneous genetic hypertension, in rats with renovascular and DOCA-salt-induced hypertension as well as the effect of high salt diet on the permeability were studied using the flame photometry method. The increase permeability of the red blood cells in the rats with spontaneous genetic hypertension was observed, while no changes occurred in the cases of DOCA-induced and renovascular hypertension. Salt load as well as deoxycorticosterone administration had no effect on the permeability of the red blood cell membrane.

Animals↗
PubMed1981

[Characteristics of the structural state of the erythrocyte membrane in rats with spontaneous genetic hypertension].

The structure of the surface and internal hydrophobic areas of the erythrocyte membranes of spontaneously hypertensive rats (SHR) was studied by means of fluorescent probes. The dependences on temperature of the fluorescence intensities of 1-aniline-naphthalene-8-sulfonate and N-phenyl-1-naphthylanine as well as the fluorescence spectra of pyrene and NN fluorescence polarization anisotropy of diphenylhexatriene wee analysed. It was found that the structure of the SHR erythrocyte membranes is altered. This alteration was interpreted as increasing of the membrane microviscosity at the areas of lipid -- protein contacts.

Animals↗
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↗