The effects of the NO donor sodium nitroprusside and the NO synthase blocker L-omega-N-nitroarginine (LNA) on body temperature, hypothalamic monoamines, and plasma corticosterone in conditions of cooling were studied in Male Wistar rats. Reductions in body temperature on cooling, both after administration of sodium nitroprusside and LNA, were no different from those seen without treatment. The basal corticosterone level after treatment with sodium nitroprusside increased from 5.3 +/- 2.2 to 29.1 +/- 1.8 microg%. Cooling led to a multiple increase in corticosterone levels in all animals, both in control conditions and after treatment with sodium nitroprusside and LNA. Sodium nitroprusside significantly decreased the basal hypothalamic noradrenaline level, by 37%. Cooling of the animals in these conditions led to an additional drop in the noradrenaline level. Noradrenaline levels 48 h after cold stress applied to animals cooled after treatment with LNA or sodium nitroprusside were significantly higher than in those cooled without treatment. No changes in serotonin and 5-hydroxyindoleacetic acid levels were seen in these experiments. The basal dihydroxyphenylacetic acid and dopamine levels increased after treatment with sodium nitroprusside, by 379% and 239% respectively. No dopamine response to cold was observed, though the dihydroxyphenylacetic acid level in the control group and animals treated with LNA increased. Thus, cold stress did not reveal differently directed directions for the actions of the NO donor and the NO synthase blocker, as seen with other types of stress.
The relationships between serum corticosterone content, intensity of lipid peroxidation (LPO) and the concentration of tocopherol in tissues, and the transmembrane potential in thymocytes were studied in rats exposed to two consecutive coolings. Both exposures increased serum corticosterone. The first exposure activated LPO in the serum, while the second stimulated LPO in thymocytes. The second cooling lowered body temperature to a lesser extent than the first one. Body temperature did not depend on the content of LPO products or corticosterone, but negatively correlated with the content of tocopherol in the brain hemispheres and adrenal glands. The rats exhibiting high-level thermoregulation after the first exposure to cold showed a higher thymocyte transmembrane potential after the second cooling. The second exposure potentiated the negative relationship between the brain and serum content of corticosterone and LPO products, which indicates that the content of LPO products cannot be used as an index of stress intensity.Key Words: cold; stress; corticosterone; lipid peroxidation; tocopherol Activation of lipid peroxidation (LPO) is the most important pathogenic event in stress causing disruption of biological membranes and uncoupling of oxidative phosphorylation. Along with the adrenal cortical hormones, LPO products are widely used as a measure of stress-response. It is currently accepted that the content of LPO products is directly proportional to the intensity of stress. However, the relationship between LPO activity and the duration and intensity of stress is not linear, and the content of LPO products can decrease during the initial phase of organism's response to stress. Such a decrease was observed at some periods of the emotional pain stress [2], during physical exercises [12] and cold exposure [5,10,11], The data indicate that the periods during which the content of LPO products in diverse organs and tissues is decreased are not synchronized [10], but coincided with an increase in the serum content of corticosteroids. The total effect of steroids is probably deterInstitute of Physiology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk mined by their antioxidant properties [9] and the modulating effects on the antioxidant system, the key stress-protecting system controlled by a variety of hormones, including corticosteroids [6,15]. Therefore, it remains unclear what is reflected by LPO changes at different stress-response periods and how these changes correlate with adrenal cortex activation.To answer these questions we used the model of repeated cooling (two 1.5-h exposures with a 48-h interval). Correlation analysis was applied to assess the relations between serum concentration of corticosterone (CS) and the content of LPO products and tocopherol in tissues. Additionally, we measured the transmembrane potential of thymocytes (Aw), which is the sum of A~ on the plasma and mitochondrial membrane. Thymocytes represent an adequate model for the assessment of the intensity of bioe...
The serotoninergic system and nitric oxide system were studied in spontaneously hypertensive rats SHR and Wistar rats (control). The contents of serotonin, 5-hydroxyindoleacetic acid (serotonin metabolite), L-arginine, monomethylarginine, and asymmetric and symmetric dimethylarginines were measured in blood plasma. Serotonin content in hypertensive animals was much higher than in Wistar rats. No interstrain differences were found in the concentration of 5-hydroxyindoleacetic acid. The concentration of asymmetric dimethylarginine in SHR rats was higher than in Wistar rats. However, the concentration of monomethylarginine in SHR rats was lower than in Wistar rats. Our results and published data on the serotoninergic system indicate that SHR rats serve as a convenient model of hypertension.
Exposure of restrained rats to cold caused a drop in rectal temperature by 3~ attenuated membrane potential by A~T, decreased the level of lipid peroxidation products, and increased the viscosity of membrane lipids in thymocytes. Although diazepam (5 mg/kg, 1 h prior to experiment) decreased A~T and lipid viscosity under comtortable temperature, it prevented the cold-induced changes in these parameters. Incubation of intact rat thymocytes with diazepam (0.2 ~tg/ml) decreased A~T, increased lipid viscosity, and did not change the intensity of lipid peroxidation. Possibilities are discussed to reduce with the help of diazepam the cold-related energy losses not only due to its effect on the central benzodiazepine receptors, but also due to changes in functional and structural parameters of the membranes caused by interaction with peripheral receptors.
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