Effect of benactyzine and arecoline on Mg2–-ATPase activity and content of Ca2– and Mg2– ions in the rat brain

The effect of the central cholinolytic benactyzine (40 mg/kg) and of the cholinomimetic arecoline (2.5 mg/kg) on activity of Mg^2–-dependent ATPase was studied and the content of Ca^2– and Mg^2– ions determined in rat brain. Benactyzine and arecoline caused biphasic changes in the activity of the enzyme and content of the electrolytes. It is concluded that inhibition of the enzyme is linked with the accumulation of Ca^2– ions and its activation with an increase in the concentration of Mg^2– ions in brain tissue. It is suggested that benactyzine and arecoline exert their influence on the liberation and retention of neuromediators in the tissue depots through these effects.(Presented by Academician of the Academy of Medical Sciences of the USSR V. V. Zakusov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol.84, No. 9, pp. 306–309, September, 1977.     

Effect of alcoholic intoxication on water content and activity of Na,K-ATPase and Ca-ATPase in rat brain

We studied the effect of 2-week alcohol intoxication on water exchange and activity of Na,K-ATPase and Ca-ATPase in rat brain. Alcohol intoxication increased water content in the brain due to cell hyperhydration. It is assumed that hyperhydration results from increased Na⁺ content in cells due to inhibition Na,K-ATPase activity, which in turn is caused by activation of lipid peroxidation under the effect of ethanol. A possible mechanism of Na,K-ATPase inhibition.     

Impact of 13(S)-HPODE,a lipoxygenase product of linoleic acid,on calcium transport and Na,K-ATPase activity in the myocardial sarcolemma

In thisin vitro study using a purified sarcolemmic fraction of guinea pig myocardium, the 13(S)-hydroperoxide of linoleic acid (13-HPODE) increased in a dose-dependent manner the permeability of myocardial sarcolemma to Ca ions in concentrations above 10 μmol/liter, stimulated Na/Ca exchange there in concentrations from 0.1 to 10 μmol/liter, and exerted a digitalis-like action on sarcolemmic Na,K-ATPase in concentrations between 0.1 and 100 μmol/liter (IC₅₀=20 μmol/liter). The results indicate that the linoleic acid hydroperoxide may be an effective modulator of sarcolemmic Ca²⁺ transport and of membrane-bound enzymes. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 120, N ^o 9, pp. 255–257, September, 1995 Presented by D. F. Chebotarev, Member of the Russian Academy of Medical Sciences     

Invertor-mediated modulation of Na,K-ATPase activity in myocardial plasma membranes in the emergency stage of compensatory cardiac hyperfunction in mature and senescent rats

Myocardial hyperfunction is experimentally modeled by coarctation of the aorta in mature (6–8-month-old) and senescent (26–28-month-old) Wistar rats. During the emergency phase of cardiac hyperfunction Na,K-ATPase activity is shown to rise reliably in mature animals, while in old rats it remains unchanged. Cardiomyocyte cytosol and blood plasma from mature (but not old) rats with experimental coarctation of the aorta activate Na,K-ATPase in membranes from the myocardium of both the mature and old rats. It is assumed that the activation of Na,K-ATPase during the emergency stage of cardiac hyperfunction is mediated through synthesis of specific invertors. In senescent animals the synthesis of invertors probably becomes insufficient, while membrane sensitivity to them is preserved. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 121, No. 6, pp. 631–633, June, 1996     

A putative inverter mechanism of hormonal Na,K-ATPase regulation

Insulin, testosterone, and thyroxine activated the Na, K-ATPase of hepatocyte plasma membranes in adult rats. Incubation of intact plasma membranes from rat hepatocytes with hepatocyte cytosol or blood serum from adult rats injected with one of the three indicated hormones led to elevated Na, K-ATPase activity in the incubated plasma membranes. It is suggested that hormones induced the appearance in liver cells and blood serum of a factor, called inverter, that is ultimately responsible for the observed Na, K-ATPase activation. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 122, No. 7, pp. 9–11, July, 1996     

Role of Na,K-ATPase in absorption of isotonic fluid by frog gall bladder epithelium

Experiments on isolated frog gall bladders showed that the addition of ouabain (1·10^–4 M) or noradrenalin (3·10^–6 M) to the incubation Ringer's solution from the side of the serous surface of the organ or replacement of the K⁺ in the solution by the equivalent Na⁺ concentration causes a decrease in the rate of absorption of fluid by the epithelium and a decrease in the Na,K-ATPase activity in its cells. Noradrenalin reduces Mg-ATPase activity also. Significant positive correlation was found between the rate of transport of isotonic fluid by the epithelium and the Na,K-ATPase activity in its cells.Department of Physiology of Water and Salt Metabolism, A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. (Presented by Academician of the Academy of Medical Sciences of the USSR N. N. Gorev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 85, No. 5, pp. 515–517, May, 1978.     

Is Na,K-ATPase the target of oxidative stress?

The susceptibility of Na,K-ATPase from bovine brain to various compounds containing active oxygen radicals is assessed. Sodium nitroprusside slightly inhibits Na,K-ATPase, while light-induced NO^o radicals (controlled by the rate of ascorbate oxidation) have no effect on the enzyme. When added in concentrations equally effective in the ascorbate oxidation assay, hydrogen peroxide and sodium hypochlorite inhibit Na,K-ATPase by 70 and 25–30%, respectively. The Fe-dinitrosyl-cysteine complex is the most potent (K_0.5=20 μM) inhibitor of Na,K-ATPase. It is demonstrated that different free oxygen radicals accumulated in the ischemic brain cause different kinds of damage to Na,K-ATPase. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 121, N ^o 3, pp. 275–278, March, 1996 Presented by I. P. Ashmarin, Member of the Russian Academy of Medical Sciences     

Opposite effects of adaptation to short-term stress and adaptation to periodic hypoxia on Na,K-ATPase activity in liver plasma membranes

Na,K-ATPase activity is shown to be lowered more than twice 2 hours after emotional pain stress in comparison with the initial level, remaining practically unchanged during the subsequent 24 hours. Adaptation to repeated stress results in a 50% activation of Na,K-ATPase. A protective effect is demonstrated in long-term stress against the background of preadaptation. Adaptation to periodic hypoxia inhibits liver Na,K-ATPase to the same extent as does acute stress. Against the background of preadaptation to periodic hypoxia, stress does not aggravate the drop of Na,K-ATPase activity. Adaptation to stress inhibits accumulation of products ofin vitro-induced lipid peroxidation in the heart 1.4-fold and does not affect it in the liver, whereas adaptation to hypoxia sharply accelerates the accumulation of oxidized products in both organs, which probably explains the activation of liver Na,K-ATPase in adaptation to stress and its inhibition in adaptation to hypoxia. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 121, No. 4, pp. 383–386, April, 1996 Presented by G. N. Kryzhanovskii, Member of the Russian Academy of Medical Sciences     

Effect of benactyzine and arecoline on the45Ca uptake by rat brain nerve endings

The effect of the central cholinolytic benactyzine and the cholinomimetic arecoline on the uptake of⁴⁵Ca by rat brain synaptosomes was studied in vitro. Benactyzine was shown to cause biphasic changes (a decrease followed by an increase) in the intensity of uptake of the isotope, whereas arecoline led to a rapid initial increase in⁴⁵Ca uptake. Benactyzine was shown to depress the effect of arecoline and depolarization on uptake of the isotope. It is concluded that the increase in⁴⁵Ca uptake through the action of arecoline is connected with activation of Nachannels. Benactyzine, on the other hand, reduces the permeability of the these channels for⁴⁵Ca and activates the Ca-channels proper.(Presented by Academician of the Academy of Medical Sciences of the USSR S. S. Golikov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 9, pp. 301–304, September, 1978.     

Effect of electric shock on activity of Na,K-ATPase and enzymes of mediator metabolism in the rat brain

Activity of Na,K-ATPase, acetylcholinesterase (AChE), and glutamate decarboxylase (GDC) was investigated in fractions of the rat brain and spinal cord during and 5 and 30 min after a single electric shock. GDC activity of the brain synaptosomes was reduced but not significantly, whereas activity of AChE, Na,K-ATPase and, probably, proteolytic enzymes was increased 5 min after electric shock and returned to normal after 30 min. It is suggested that inhibition of Na,K-ATPase activity in the synaptosomes of the rat cerebral cortex may play a role in the pathogenesis of convulsions.Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. Kemerovo Medical Institute. (Presented by Academician of Medical Sciences of the USSR G. N. Kryzhanovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 8, pp. 139–142, August, 1978.     

Impact of ammonium chloride in a toxic dose on the bioelectrical activity of rat brain

Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 116, N ^o 7, pp. 19–21, July, 1993     

Effect of electric shock and diazepam on of Na,K-ATPase activity in brain membranes

The phenomenon of inactivation of Na,K-ATPase of the unpurified synaptosomal fraction from rat cerebral cortex in electric shock may be connected with modification of the potassium combining site of the enzyme. The anticonvulsant diazepam, if injected intramuscularly, also inhibits the Na,K-ATPase of the brain membranes, but diazepam followed by electrical stimulation of the brain in vivo activates Na,K-ATPase by comparison with the control. Diazepam also abolishes clonic convulsions following electrical stimulation of the brain. Meanwhile diazepam does not abolish the compensatory changes in acetylcholinesterase activity of brain and spinal cord synaptosomes of rats with electric shock. The results are discussed in connection with the view that inhibition of Na,K-ATPase activity of the nerve ending membranes may be the pathogenetic mechanism of seizure activity.Laboratory of General Pathology of the Nervous System, Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. Department of Biochemistry. Kemerovo Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR A. M. Chernukh.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 87, No. 3, pp. 204–207, March, 1979.     

Effect of low-intensity laser radiation on capillaries in the rat brain

Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny Vol. 115, N ^o 2, pp. 219–221, February, 1993