[Reactive nitrogen and oxygen species metabolism in rat heart mitochondria upon administration of NO donor in vivo].

Some aspects of reactive nitrogen and oxygen species (RNS and ROS) metabolism in rat heart mitochondria under administration of different doses of nitroglycerine (NG) in vivo are discussed. It is shown that NG administration results in a dose-dependent increase in Ca2+-uptake in mitochondria, due to the dose-dependent inhibition of mitochondrial permeability transition pore (MPTP) in vivo and the activation of Ca2+-dependent mitochondrial NOS. It was shown that NOS activity increases in accord with the increase of Ca2+-uptake in mitochondria.

[Arginase-nitric oxide synthase system changes due to adaptation to swimming in adult and aged rat hearts].

We tested the physiological indices of adult rat heart beat for the adaptation to prolonged physical exercise (swimming). It was shown that the stimulation of NO-production in the heart mitochondria of trained adult rats improves both systolic and diastolic heart function. In adult rats trained by swimming the activity of both de novo and salvage enzymes of nitric oxide synthesis studied (iNOS, cNOS, nitratreductase) were increased in heart mitochondria, whereas in the old rats only the activity of oxidative de novo enzymes.

[Magnetic-laser influence on the system of nitric oxide and contractile activity of smooth muscles of rat aorta under hypertension].

The study was conducted on three groups of rats: Group I included Wistar rats with normal blood pressure (first control group); group II - rats with genetically determined hypertension (second control group); group Ill - rats with genetically determined hypertension under the influence ofmagnetic-laser power (study group). For the low-intensively magnetic-laser influence (MLI) we have used device MIT-MT, Ukraine, which was designed for the treatment of low-frequency magnetic field using optical flow blue and red ranges of spectrum. The MLI duration was 15 minutes for the blue range, and 25 minutes for the red one.

[Mitochondria permeability transition as a target for ischemic preconditioning].

The ischemic preconditioning (IPC) limits myocardial injury provoked by a subsequent prolonged ischemia-reperfusion (I/ R). The underlying mechanisms of enhanced resistance of heart are actively studied, but for sure it was established that mitochondria play a major role in IPC-stimulated adaptation to ischemia. In this article we present and discuss evidences that cardioprotective effect of IPC is mediated by inhibition of mitochondria permeability transition pore (MPTP) opening.

[The effect of hydrogen sulfide on contractile activity of the vascular smooth muscles in rats].

The effect of endogenous and exogenous hydrogen sulfide (H2S) on contractile activity of vascular smooth muscle (VSM) was studied. The introduction of substrate synthesis H2S L-cysteine and its donor NaHS in vitro caused concentration-dependent relaxation of VSM of aorta and portal vein. Low concentrations of hydrogen sulfide donor (10(-5) mol/L) caused vasoconstriction of both types of the vessels.

[The role of mitochondria in NO-dependent regulation of Na+, K+ -ATP activity in the rat aorta].

In experiments in vivo we studied the interaction between two ion-transporting mechanisms of cardiovascular system--Na+, K+ -ATPase of rat aorta and Ca2+ -uptake system of mitochondria in short-term response to different doses of NO donor, nitroglycerine (NG). The activity of the Na+, K+ -ATPase was determined in rat aorta, and mitochondrial uptake of Ca2+ was studied in rat heart mitochondria assuming that metabolism induced by NO in cardiac mitochondria is similar to that in rat aortic mitochondria. The data show a coordinated dose-dependent action of NG on Na+, K+ -ATPase activity as well as Ca2+ -uptake in mitochondria.

[Oxidative stress in the cardiovascular system of rats with chronic deficiency of cerebral dopamine].

The physiological significance of cardiac mitochondrial reactive oxygen species (ROS) regulation is unknown. In the current study, mitochondrial ROS (O2- and OH) generation, stable H2O2 and lipids peroxidation marker (malonic dialdehyde, MDA) pools, as well as pools of potent antioxidants--urea and uric acid--were determined in rat heart, miocardial mitochondria and in blood plasma and erytrocytes at low (44%) and high (96%) levels of cerebral dopamine-synthesis neurons destruction (by 6-hydroxidopamine treatment). In the untreated rats, ROS generation, H2O2 and MDA levels were low but in rats with chronic (3-4 month) deficiency of cerebral dopamine synthesis by nigro-striatal dopaminergic system, ROS generation and lipids peroxidation were progressively increased.

[Effect of nitric oxide on Na+, K(+)-ATPase in the aorta tissue of rats].

The influence ofnitric oxide on Na+,K(+)-ATPase activity in rat aorta was studied by means of stimulation of endogenous NO synthesis after injections of bacterial lipopolysaccharide (LPS) and pharmacological NO donor nitroglycerine (NG). It was shown that NO action on Na+,K(+)-ATPase in vivo is dose-dependent. Stimulation of the endogenous NO synthesis by LPS as well as the administration of low doses of NG lead to the activation of Na+,K(+)-ATPase and favor the conclusion that NO-dependent Na+,K(+)-ATPase stimulation mediates vasodilatory and hypotensive action of nitric oxide.

[Effects of uncoupling proteins on nitric oxide synthesis and oxidative stress development in ishemia-reperfusion of old rat hearts].

Genipin is aglycone of geniposide, one of the active compounds of Gardenia gasminoides Ellis. The gardenia fruit extract has been used in traditional Chinese medicine to relieve the symptoms of type 2 diabetes that is accompanied with extensive oxidative stress and endothelial dysfunction of NO production. Besides, genipin was shown to inhibit UCP-depended proton leak through the inner mitochondrial membrane that leads to increased membrane potential and ATP production.

[The inhibition of oxidative and nitrosative stresses by ecdysterone as the mechanisms of its cardio- and vasoprotective action in experimental diabetes type I].

Streptozotocine (STZ) administration (5 mg/100 g) up regulates oxidative (lipid peroxidation as a marker) and nitrosative (protein nitrosilation as a marker) stresses as well as ROS (O(2-), H2O2, OH) generation in heart and aorta in rats after 60 days of STZ action. The level of oxydative stress was higher in aorta. Xanthine oxidase (XO) activation (uric acid as marker), but not lipoxygenase (LTC4 as marker) or cyclooxygenase (TxB2 as marker) are the main oxydases that generate O(2-) as calculated by correlation analysis.

[Mitochondrial permeability transition pore opening inhibition by ecdysterone in heart mitochondria of aging rats].

Nitric oxide reacts rapidly with superoxide to produce the potent oxidant peroxynitrite. In vivo mitochondria produce superoxide as well as NO. In heart mitochondria of aging rats the amount of NO and O2(-) are increased thus the levels of peroxynitrite produced may be increased too, in this reason mitochondria may be a major site of peroxynitrite formation.

[Role of non-haem iron in protecting effect of ecdysterone on development of streptozocin-induced hyperglycaemia in rats].

Chronic hyperglycaemia (60 days) which developed after streptozotocine (STZ) administration (5 mg/100 g) in rats was accompanied with development of severe endothelial dysfunction as well as with disturbed non-haem iron metabolism. It was established by EPR spectroscopy method that STZ administration reduced transferrin levels in the blood as well as pools of iron associated with blood transferrin and with ferritin in the heart and aorta of rats with hyperglycaemia. Chronic ecdysterone administration (100 ng/100 g, 60 days) protects hyperglycaemia development by preventing of non-haem iron metabolism disturbance.

[Modulating effect of Serratula coronata extract on nitric oxide metabolism in the aorta tissues of rats in lead intoxication].

Vasotoxic effect of prolonged lead exposures and the efficiency of vasoprotective effect of S. coronata extract per os addition is estimated in rats aorta It is established that lead in aorta causes a significant increase in reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation by increasing the activity of inducible isoform of NO-synthase (iNOS). The use of S.

[The role of nitric oxide and superoxide synthesis in protective mechanism of ecdysterone in the heart mitochondria of rats with streptozotocin-induced diabetes].

This study evaluated generation of O2*- and NO in heart mitochondria isolated from 9-week old streptozotocin (STZ)-induced diabetic rats and the effect of ecdysterone treatment on these parameters. Mitochondria isolated from 9-week old placebo-treated rats were used as control. Several parameters were evaluated: O2*- production, the levels of stable NO metabolites nitrate, nitrite and total nitrosothiols, the level of bilirubine (as marker of CO generation), inducible (iNOS) and constitutive (nNOS) mtNOS, NADH- dependent nitrate reductase (NR) and inducible arginase II (AII) activity.

[Effect of enalapril on nitric oxide synthesis, oxidative metabolism, and vascular tone in aging rats].

Endothelium-dependent and endothelium-independent reactions of relaxations of vascular smooth muscle (VSM) were examined in the aorta preparations of the two groups (6-8 and 21-22 month). The studies also two NO synthase (NOS) isoform activity--inducible (iNOS) and constitutive (cNOS), activity of arginase and nitrate reductase and the content of high-molecular nitrosothiols (HMNT) and low-molecular nitrosothiols (LMNT) and stable metabolites of NO (NO(-)2, NO(-)3). Aging rats demonstrated only endothelium-dependent responses of VSM to acethylcholine lowering.

[NO-dependent mechanisms of ecdysterone protective action on the heart and vessels in streptozotocin-induced diabetes mellitus in rats].

Ecdysterone (100 ng/100 g) chronic oral administration (2 months after STZ (5 mg/100 g) administration) normalized plasma glucose levels in rats. This potent hypoglycemic effect of ecdysterone depend on inhibition of non-constitutive NO synthesis by Ca(2+)-independent iNOS and NADP-dependent nitrate reductase as well as inhibition of L-arginine degradation by arginase result in up-regulation of Ca(2+)-dependent constitutive NO synthesis by eNOS or mithochondrial nNOS in heart and aorta of rats.