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G M Boriskina

Publications and source records attributed to G M Boriskina.

13 recordsLinked to original sources
PubMed1980

[Characteristics of 3H-dihydroalprenolol binding to beta-receptors in the fat cells of rats and spontaneous genetic hypertension and in hypertensive disease].

The binding of 3H-dihydroalprenolol, a beta-antagonist, with the fat cell plasma membrane was studied in spontaneously hypertensive rats and in patients with essential hypertension. It was found that, as compared to control rats, hypertensive animals had an increased maximum number of 3H-DHA binding sites in the membranes and diminished affinity of beta-adrenoreceptors. It is suggested that these differences may play an essential role in the latered sensitivity to adrenalin in hypertensive rats. Removal of the adrenal, i. e. deprivation of the stabilizing corticosteroid effect, leads to marked changes in the state of the beta-adrenoreceptors in hypertensive animals. Thus, the maximum number of binding sites reduces in hypertensive rats but remains unaltered in the controls; following adrenalectomy the affinity of beta-adrenoreceptors increases in rats with hypertension, but in normal rats, on the contrary, does not change or rather has a tendency to decrease.

Adipose Tissue↗
PubMed1979

[Effect of the beta-adrenoblocker propranolol on adrenaline-stimulated lipolysis in the adipose tissue of spontaneously hypertensive rats].

The effect of the beta-adrenoblocker propranolol on adrenaline-stimulated lipolysis was studied in the adipose tissue of spontaneously hypertensive rats (SHR) and control rats. The lipolytic activity was estimated from the increase in glycerol concentration in the incubation medium in vitro. The adipose tissue of SHR responded to adrenaline similarly to that of control rats, but the concentration of adrenaline inducing the half-maximum response (KA) was 2 times less for SHR than KA for normotensive controls. Under propranolol effect this parameter was increased more significantly in SHR than in controls. These data indicate higher sensitivity of SHR adipose tissue to propranolol that may well be relative to alteration of the properties of beta-adrenergic receptors of adipose tissue in this form of hypertension.

Adipose Tissue↗
PubMed1977

[Effect on some pyridine derivatives on the activity of heart NAD glycohydrolase].

Effect of some 3- and 4-substituted pyridines on enzymatic hydrolysis of NAD by rabbit heart muscle NAD-glycohydrolase has been studied. It is shown that some 4-substituted derivatives in contrast with 3-substituted ones produce an inhibitory effect on the enzyme activity. A new efficient inhibitor of rabbit heart muscle NAD-glycohydrolase (I50 = 10(-3) M)--N1-(2-lactyl)-N2-(isonicotinoy)hydrazine, inducing uncompetitive inhibition of hydrolysis of NAD is found. The mechanism of the inhibitory effect of N1-(2-lactyl)-N2-(isonicotinoyl)hydrazine was investigated and the rate equation for enzymatic hydrolysis of NAD in the presence of inhibitor is calculated. It is suggested, that the inhibitory effect of N1-(2-lactyl)-N2-(isonicotinoyl)hydrazine is due to the formation of triple inactive complex inhibitor-enzyme-adenosinediphosphateribose.

Adenosine Diphosphate Sugars↗
PubMed1977

[Phosphoinositide content in the erythrocyte membranes of rats with spontaneous hypertension].

The values of triphosphoinositides (TPI) and monophosphoinositides (MPI) contents per 1 mg of membrane protein in the erythrocyte hosts of spontaneously hypertensive rats (SHR) constitute 178 and 74%, respectively, of that in the erythrocyte hosts of normotensive rats (NR). The total amount of phosphoinositides in the erythrocyte hosts of NR is more than 120% of the total amount of these lipids, in the erythrocyte hosts of SHR.

Animals↗
PubMed1976

[Natriuretic factor].

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Adenosine Triphosphatases↗
PubMed1975

[Na+--K+-adenosine triphosphatase and some oxidoreductases in the kidney of rats with spontaneous hypertension].

The activities of the Na+--K+-ATPase, succinic dehydrogenase (SDH/, lactic dehydrogenase (LDH/ and glucose-6-phosphat dehydrogenase (G-6-PDH/ were studied in the cortex outer and inner medulla of the kidneys of rats with spontaneous hypertension (SHR) and were compared with those of control normotensive Wistar rats. The SHR aged 6--8 weeks had durint the prehypertensive and the early hypertensive stage the same enzymatic activities as control rats. Rats with a steady SH aged 16-22 weeks had low specific activity of the, Na+--K+-ATPase, SDH and LDH in the outer medulla. The latter can be associated with decreased intensity of the energy metabolism and a reduction of the active sodium transport in the ascending limb of the loop of Henle in the SHR rats and cold cause the phenomenon of exaggerated natriuresis characteristic of hypertension.

Adenosine Triphosphatases↗
PubMed1975

[Solubilization and several properties of NAD-glucohydrolase isolated from rabbit heart].

Methods of isolation of NAD-glucohydrolase from the fraction of heart microsomes were searched for. NAD-glucohydrolase proved to pass into a soluble state under the effect of phospholipase A, triton X-100 and Na cholate. NAD-glucohydrolase was found to possess peculiar properties; it reversibly became denatured under the effect of 6M urea, but failed to become inactivated with own substrate (NAD) at pH 8.0. In case of NAD-ases isolated from other sources the reversible denaturation by means of urea as a rule correlated with the enzyme inactivation in the presence of NAD at pH 8.0.

Animals↗