Role of glutathione in stabilization of nitric oxide during hypertension developed by inhibition of nitric oxide synthase in the rat

The present study examined the role of glutathione in the development of hy pertension induced by long-term inhibition of nitric oxide (NO)-synthase. T hree groups of rats were investigated: control group, L-NAME group: group w ith NO-synthase inhibition by N-G-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg per day) for 2 weeks, and BSO group: group with glutathione synthesi s 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 gi ven substances were exchanged between groups. There was no change in systol ic 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, SEP increased significan tly by 10% after 2 h of acute BSO treatment. In the BSO group, SEP did not change vs control; however, after 2 h of acute L-NAME (10 mg/kg, i.v.) trea tment, the increase in SEP exceeded by 12% (P<0.05) that of the control gro up. Along with the increase in SEP, acute BSO treatment significantly poten tiated the decrease in plasma nitrite/nitrate concentration in the L-NAME g roup. 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 an d a stabilizing role of glutathione.