This review summarizes our findings concerning the altered balance of vasoactive systems (namely sympathetic nervous system and nitric oxide) in various forms of experimental hypertension – genetic hypertension (SHR, HTG rats), salt hypertension (Dahl rats) and NO-deficient hypertension (L-NAME-treated rats). An attempt is made to define relative NO deficiency (compared to the existing level of sympathetic vasoconstriction), to describe its possible causes and to evaluate particular indicators of its extent. A special attention is paid to reactive oxygen species, their interaction with NO metabolism, cell Ca2+ handling and blood pressure regulation. Our current effort is focused on the investigation of abnormal regulation of cytosolic Ca2+ levels in smooth muscle and endothelium of hypertensive animals. Such a research should cl
arify the mechanisms by which genetic and/or environmental factors could chronically modify blood pressure level.
The erythrocytes represent an important source of antioxidant capacity of the blood. Catalase (EC 1.11.1.6.) is one of the enzymatic components of their antioxidant defense system. The objective of this study was to follow erythrocyte catalase (CAT) in 7-, 15-, 21-, 35-, 60- and 90-day-old Wistar rats of both sexes in normoxia and after exposure to intensive acute hypobaric hypoxia. During the development CAT activity increases in both sexes, but the rise was usually higher in females. Hypobaric hypoxia increased CAT activity in all studied age groups of both sexes. However, higher CAT activity in females was less affected by hypoxia than the lower activity in males. This was true for nearly all age groups studied. It can be concluded that both ontogenetic aspects and sex differences play a major role in establishing the activity of CAT, which is an important part of the antioxidant defense of the organism.
Our study addresses selected parameters of rat erythrocyte ion transport (Na+-K+ pump, Na+-K+-2Cl- cotransport, and passive cation fluxes) after acute or chronic hypoxia exposure. We did not find any significant change of ion transport after acute hypoxia. However, chronic hypoxia could modify ion transport because the affinity of Na+-K+ pump for intracellular Na+seems to be decreased.
Coenzyme Q (CoQ), a lipophilic substituted benzoquinone, is well known as a redox component of the mitochondrial and many bacterial respiratory chains. However, additional locations and roles have been recently discovered. CoQ is described as a redox component of extramitochondrial electron transport chains and it is a powerful antioxidant and a membrane stabilizer. Increasing evidence for the beneficial clinical effects of CoQ administration in senescence or in different disorders (e.g. cerebrovascular, muscular, neurogenic) may be explained by the multiple roles of CoQ in cells.
The extent of ADP.Fe/NADPH-induced lipid peroxidation measured as production of thiobarbituric acid-reactive substances (TBARS) was determined in isolated membranes from cerebral cortex, heart and kidney of 21-days- old rats. The time course of lipid peroxidation showed higher production of TBARS in cerebral cortex than in heart and kidney. Our data indicate that high level of TBARS production is not due to high activity of NADPH oxidoreductase but due to high content of endogenous lipids in cerebral cortex membranes that could be modified. Higher production of TBARS in cerebral cortex is the result of higher content of lipids in cerebral cortex membranes because NADPH cytochrome c reductase activity in membranes of cerebral cortex is lower than that of heart and kidney.
Carnitine administration (by intraperitoneal injection) to 21-day-old-rats prevents the increase of thiobarbituric acid-reactive substances (index of lipid peroxidation and free radical damage) induced by 30 min hypobaric hypoxia in four different parts of the brain (cerebral cortex, subcortical structures, medulla oblongata and cerebellum).
Mitochondria were isolated from regenerating rat liver 12, 24 and 48 h after partial hepatectomy. The "State 3" and "State 4" respiration were measured in the presence of succinate. The P/O quotient and respiratory control index (RCI) were calculated. The experimental data showed that the partial uncoupling of oxidative phosphorylation in regenerating liver mitochondria occurring in the early period of regeneration is partly due to free fatty acids.
Glycerol-3-phosphate oxidation in brown adipose tissue mitochondria of cold-adapted hamster is strongly inhibited by phospholipase A2 (PLA2)- Our data show that the glycerol-3-phosphate branch of the respiratory chain is sensitive to PLA2 action more than the succinate branch and that the transfer of reducing equivalents from the glycerol-3-phosphate dehydrogenase to arteficial electron acceptor is especially sensitive to the PLA2 action.
The recovery of total DNA content and recovery of total cytochrome c oxidase activity in the rat liver after partial hepatectomy is accelerated by triiodothyronine applied in three doses, two before and one immediately after liver resection. Triiodothyronine-treated animals already have higher cytochrome c oxidase activity before resection. The recovery of the tissue oxidative capacity after partial hepatectomy is more rapid in triiodothyronine-treated animals. These data indicate that hormonal activation of the liver regeneration process is involved.