PubMed Health⌕ Search

Biomedical subjects

O M Bukhanevich

Publications and source records attributed to O M Bukhanevich.

10 recordsLinked to original sources

[Effect of irbesartan, an antagonist of AT-1 receptors for angiotensin II, on L-arginine metabolism in arterial hypertension].

Effects of an antagonist of AT-1 receptors for angiotensin-II (Ang-II) irbezantane on the NO-synthase and arginase ways of the metabolism of L-arginine were studied in plasma and erythrocytes of the patients with arterial hypertension. The intensity of the non-oxidative arginase way of L-arginine metabolism in plasma and erythrocytes has been shown to be inhanced at hypertension versus the normotensive patients, while the activity of the alternative oxidative NO-synthase way was reduced. Inhibiting AT-1 receptors for Ang-II with high-affinity antagonist irbezantane normalized the ratio between two alternative ways of L-arginine metabolism through inhibiting the arginase way and reciprocal activating the NO-synthase way both in human plasma and erythrocytes.

Angiotensin II↗

[Increased level of nitric oxide stable metabolites in the blood of highlanders].

The investigation was designed to study nitric oxide (NO) blood level estimated by measuring its stable metabolites nitrite (NO2-) and nitrate (NO3-) concentration in highlanders (2,200 m a.s.l.). NO2- [symbol: see text] NO3- concentration was measured with Griss reagent and brucine reagent respectively with using the spectrophotometric method. We first found that highlanders compared to lowlanders have increased blood level of NO2- (37 +/- 3.3 nmol/ml vs. 28.5 +/- 1.3 nmol/ml, P < 0.05) and NO3- (1362 +/- 43 nmol/ml vs. 845 +/- 65 nmol/ml, P < 0.001). As the most significant, there was increase in NO2- concentration in erythrocytes (by about 6 times), NO3- level in erythrocytes was revealed to be increased by 2.5 times, whereas the plasma concentration of these stable metabolites was the same (for NO3-) or even slightly decreased (for NO2-). Such increased NO stable metabolites blood level in highlanders may explain widening of vasodilative reserve and strengthening of cardiac pump and contractile functions, which we revealed previously. Activation of NO-system in high altitude is important and probable trigger adaptive mechanism of cardiovascular system to hypoxia. This mechanism allows to retain adequate tissue perfusion and optimal oxygen supply in its decreased partial pressure in inhaled air and thereby to prevent diseases caused by vasospastic processes.

Acclimatization↗

[Effect of irbesartan--angiotensin II type I receptor inhibitor on oxidative metabolism of lipids in essential hypertension].

We evaluated the alters in plasma vasoconstriction eicosanoids (LTC4, TXB2) and diene conjugates (DC) levels in patients with essential hypertension (EH) after chronic (30 days, 235 mg per day) of irbezartane (inhibitor of ANG II type 1 receptor with prolongation action "Aprovel" from "Sanofi") oral administration. Patients with EH have significantly higher plasma both LTC4, TXB2 and DC levels then healthy controls. This imbalance can be beneficially modulated by chronic irbezartane ("Aprovel") administration. It is concluded that ANG II type 1 receptors can be involved in regulation of free arachidomc acid oxidation.

Angiotensin Receptor Antagonists↗

[A chronic hyperimmunocomplex process and its interrelationship with free radical-generating systems].

On chronic hyperimmunocomplex process (CHIP) model in rats of Wistar line (Cochrane C., Koffen D., 1973) we determined cAMP and cGMP concentration, nitrogen oxide (NO), urine, urine acid,--in muscle and clearance organs, and also in plasma. In result of carried out investigations there was determined the increase of large and middle CIC in blood plasma, their fixation on endothelium of aorta bifurcation and glomerula basal membrane, partially on liver cells. There was revealed considerable disbalance of cyclic nucleotides concentration in kidneys homogenates, spleen and plasma, with guanils fall (adenil index, what is interconnected with NO level lowering in all cases and urine increase in plasma, simultaneously with its decrease in number--in kidneys and spleen. Urinic acid increased in number in kidneys, spleen, plasma. These changes create favourable background for damaging of endothelium-neutrophil-thrombocyte cooperation through hemokinin, moleculo-adhesive, fermentative mechanism with further development of proliferative-remodulating processes in vessel wall.

Animals↗

C(27)-steroid hormones calcitriol and ecdysterone activates hydrolysis of neutral lipids--cholesterol esters and triacylglycerols--in its early pregenomic phase of action.

We have examined in vivo capacities of two C27-steroid hormones-phytoecdysteroid ecdysterone (20-hydroxyecdysone, 10(-8)M) and calcitriol (1 alpha, 25-dihydroxyvitamin D3, 10(-12)M), as a modulators of neutral lipids hydrolysis in the brain and heart cells. Severe lines of evidence indicate that both hormones may acts as positive regulators of cholesterol esters and triacylglycerol hydrolysis in early (0.5-30 min) pregenomic phase of its actions, yielding known (DAG, free polyunsaturated fatty acids) and possible (free cholesterol) lipid second messengers.

Animals↗

The C(27)-steroid hormones calcitriol and ecdysterone in the early phase of its action activates hydrolysis of phosphatidylcholines in target animal tissues.

We have examined in vivo the capacities of two C27-steroid hormones--phytoecdysteroid ecdysterone (20-hydroxyecdysone, 10(-8)M) and calcitriol (1 alpha, 25-dihydroxyvitamin D3, 10(-12)M), as a modulators of phosphatidylcholine hydrolysis in the brain and heart cells of rats. Sever lines of evidence indicate that both hormones may acts as positive regulators of membrane phosphatidylcholine hydrolysis by phospholipases A2, C and D in early (0.5-30 min) membrane phase of its actions, yielding known lipid second messengers (diacylglycerol, phosphatidic acid) and soluble products, that may acts as second messengers (choline,choline phosphate, glycerophosphocholine).

Animals↗

[The C(27)-steroid hormones ecdysterone and calcitriol activate the phosphoinositol cycle in its membrane phase].

We have examined in vivo the capacities of two C27-steroid hormones-phytoecdysteroid ecdysterone (20-hydroxyecdysone, 10(-8) M) and calcitriol (1 alpha, 25-dihydroxyvitamin D3, 10(-12) M), as a modulators of phosphoinositide cycle in the brain and heart cells. Severe lines of evidence indicate that both hormones may acts as positive regulators of phosphoinositide hydrolysis by phospholipases C and D in membrane (0.5-30 min) pre-genomic phase of its actions. Thus, our findings identify ecdysterone, like calcitriol, as a positive regulator of [Ca2+]i, and protein kinase in the mammalian cells.

Animals↗

[Mechanisms of the early effect of biologically active hydroxysterols: calcitriol and ecdysterone. Modulation of intracellular pools of arachidonic acid and products of its oxidative metabolism].

It is established that ecdysterone (20-hydroxyecdysone) in concentration of 10(-8) M and calcitriol (1 alpha, 25-dihydroxyvitamin D3) in concentration 10(-12) M evoke in the studied tissues-targets of rats (brain, heart, liver, intestine mucosa) rapid (0.5-2 min) transit (2.5-4 times) increase of the intracellular pools of arachidonic acid, eicosanoid--total peptidoleukotrienes C4/D4/E4 (2.5-6 times), and, especially prostaglandins--stable metabolite prostacyclin 6-ketoprostaglandin F1 alpha (10-400 times). Ecdysterone in concentration 10(-11)-10(-9) inhibits arachidonic cascade in the brain and heart. Activation of arachidonic cascade and further increase of biosynthesis of cGMP are considered as a single negative link of autoregulation of activity of phospholipid-dependent signal system of cells and ecdysterone as a possible efficient modulator intracellular pools of eicosanoid in the tissues of warm-blooded animals.

Animals↗

[Mechanisms of the early effect of biologically active hydroxysterols: calcitriol and ecdysterone. Identification of sphingomyelin as the effector mechanism of the early effect].

Variations of sphingomyelin metabolism in the tissue of brain, liver, heart and mucosa of small intestine of healthy rats were studied in the in vivo experiments using L-[methyl-3H]methionine for 1h after administration of 10(-8)-10(-12) M of biologically active hydroxysterols--steroid hormones: ecdysterone (20-hydroxyecdysone) and calcitriol (1 alpha, 25-dihydroxy vitamin D3). Considerable activation (5-10 times) of sphingomyelin hydrolysis is observed 1-2 min after peroral administration of hydroxysterols. An essential increase of the pools of sphingosin is observed. Sphingosin is a modulator of activity of protein kinase C taking part in the transfer of the external signal to the cell. It is supposed that sphingomyelin metabolism modulation can be one of the effector mechanisms of early (pregenom) action of steroid hormones--ecdysterone and calcitriol.

Animals↗

[Mechanisms of the early effect of biologically active hydroxysterols: calcitriol and ecdysterone. Modulation of systems which generate low molecular weight activators of guanylate cyclase].

Three metabolic channels producing active forms of oxygen (OH.), carbon (CO) and nitrogen (NO) were studied for their contribution to the mechanism of early activation of guanylate cyclase by hydroxysterols: ecdysterone (20-hydroxyecdysone) and calcitriol (1 alpha, 25-dihydroxyvitamin D3) which are steroid agonists of phospholipid signal system in target tissues. It is established that in the cells of target tissues (brain, heart, liver) affected by the mentioned hydroxysterols only NO- and CO- metabolic lipid channels are activated while the nucleotide metabolic channel of generation of OH--radical is blocked. It is supposed that the nucleotide OH. metabolic channel activation due to oxidation of oxypurines and dihydroorotic acid most probably takes no part in formation of the negative feedback and termination of the signal of phospholipid signalling system by means of activation of soluble guanylate cyclase in contrast to the lipid channel of OH. formation due to oxidation of arachidonic acid.

Animals↗