Acetylcholine affects rat liver metabolism via type 3 muscarinic receptors in hepatocytes.

Although the role of acetylcholine (Ach) in hepatic glucose metabolism is well elucidated, it is still unclear if it influences gluconeogenesis, glycogenolysis and high-energy phosphate metabolism, and if it does what the mechanisms of this influence are. Therefore, using isolated perfused rat liver as a model, we have studied the effect of Ach on oxygen consumption, synthesis of glucose from lactate and pyruvate, glycogen formation, mitochondrial oxidative phosphorylation and ATP-synthesis. We have established that effects of Ach on oxygen consumption depend on its concentration. When used at a concentration of 10(-7) M, Ach exerts maximum stimulatory effect, while its infusion at 10(-6) M causes a decrease of oxygen consumption by the liver. Moreover, when used at a concentration of 10(-6) M or 10(-7) M, Ach increases rates of glucose production from the gluconeogenic substrates lactate and pyruvate, leading to enhanced glycogen content in perfused liver. It was also shown that Ach possesses a stimulating effect on alanine and aspartate aminotransferases. As detected by 31P NMR spectroscopy, continuous liver perfusion with pyruvate and lactate in the presence of Ach leads to a significant decrease of ATP level, implying enhanced energy requirements for gluconeogenesis under these conditions. Elimination of the described effects of Ach by atropine, the antagonist of muscarinic receptors, and identification of the type 3 muscarinic receptors (m3) in isolated hepatocytes as well as in whole liver, imply that Ach may exert its effect on liver metabolism through m3 receptors.

[Effect of L-arginine and the nitric oxide synthase blocker L-NNA on calcium capacity in rat liver mitochondria with differing resistance to hypoxia]. / Vplyv L-arhininu i blokatora syntazy oksydu azotu L-NNA na kal'tsiievu iemnist' mitokhondrii pechinky shchuriv z riznoiu rezystentnistiu do hipoksiï.

The effect of L-arginine and blockator of nitric oxide synthase L-NNA on processes of calcium mitochondrial capacity in liver with different resistance to hypoxia in the experiments with Wistar rats has been studied using the followrng substrates of energy support: succinic, alpha-ketoglutaric acids, alpha-ketolutarate and inhibitor succinatedehydrogenase malonate. As well we used substrates mixtures combination providing for activation of aminotransferase mechanism: glutamate and piruvate, glutamate and malate. It has been shown that L-arginine injection increases calcium mitochondrial capacity of low resistant rats using as substrates the succinate and alpha-ketoglutarate to control meanings of high resistance rats. Effects of donors nitric oxide on this processes limit NO-synthase inhibitor L-NNA.

[The effect of sodium alpha-ketoglutarate on the indices of the peripheral blood and lipid peroxidation and on the enzyme activity of antioxidant protection in irradiated rats]. / Vplyv al'fa-ketohlutaratu natriiu na pokaznyky peryferychnoi krovi, perekysnoho okysnennia lipidiv i aktyvnist' fermentiv antyoksydantnoho zakhystu oprominenykh shchuriv.

The influence of chronic roentgen irradiation in low doses on rats' quantitative and qualitative indices of peripheral blood, on lipid peroxidation and on erythrocyte antioxidant enzymes activity has been studied. It was shown that chronic roentgen irradiation in low doses had a destabilizing influence on leucocytes correlation, activated lipid peroxidation, depressed activity of erythrocytes antioxidant enzymes. Alpha-ketoglutarate injection in therapeutic doses normalized blood indices, limited the intensity of lipid peroxidation and activated antioxidant system enzymes.