Ol'ga Pechanova1, Misato Kashiba2 and Masayasu
1Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Sienkiewiczova 1, 813 71 Bratislava, Slovak Republic
2Department of Biochemistry, Osaka City University Medical School, Osaka 545 - 8585, Japan
Abstract: The present study examined the role of glutathione in the development of hypertension induced by long-term inhibition of nitric oxide (NO)-synthase. Three groups of rats were investigated: control group, L-NAME group: group with NO-synthase inhibition by NG-nitro-l-arginine methyl ester (L-NAME, 40 mg/kg per day) for 2 weeks, and BSO group: group with glutathione synthesis inhibitor l-buthionine sulfoximine (BSO, 1.4 mmol/kg per 12 h) for 3 days. All the groups were subjected to an acute i.v. experiment in which the given substances were exchanged between groups. There was no change in systolic blood pressure (SBP) in the control group after 1 and 2 h of acute BSO (1.4 mmol/kg, i.v.) treatment. In the L-NAME group, SBP increased significantly by 10% after 2 h of acute BSO treatment. In the BSO group, SBP did not change vs control; however, after 2 h of acute L-NAME (10 mg/kg, i.v.) treatment, the increase in SBP exceeded by 12% (P<0.05) that of the control group. Along with the increase in SBP, acute BSO treatment significantly potentiated the decrease in plasma nitrite/nitrate concentration in the L-NAME group. The acute BSO-induced glutathione decrease was significantly greater in the L-NAME group than in the control group. In NO-deficient hypertensive rats, the results are indicative of a decrease in glutathione synthesis and a stabilizing role of glutathione.
Keywords: Glutathione, Nitric oxide (NO), NO-synthase, NG-nitro-l-arginine methyl ester, Hypertension