Interaction of exercise training and chronic NOS inhibition on blood pressure, heart rate, NO and antioxidants in plasma of rats.
Many individuals with cardiovascular diseases undergo periodic exercise conditioning with or without medication. Therefore, the purpose of this study was to examine the effect of exercise training on BP and HR under the condition of NOS inhibition and to clarify the mechanism of the effect in regard to oxidative stress, antioxidant enzyme activity, and NO production in the plasma of the rat. Fisher 344 rats were divided into four groups: (1) sedentary control, (2) exercise training for 8 weeks, (3) nitro-L-arginine methyl ester (L-NAME) (10mg/kg, s.c. for 8 weeks) and (4) ET + L-NAME. Blood pressure (BP) and heart rate (HR) were monitored weekly for 8 weeks. The animals were sacrificed 24h after last treatments, plasma isolated and analyzed. The results show that exercise conditioning resulted in enhanced NO production (120% of control), GSH levels (110% of control), GSH/GSSG ratio (124% of control) and the up-regulation of catalase (CAT) (225% of control), glutathione peroxidase (GSH-Px) (161% of control), glutathione reductase (GR) (142% of control) and glutathione-S-transferase (GST) (189% of control) and depression of malondialdehyde (MDA) (90% of control) and lactate (75% of control) in plasma of the rat. These biochemical changes were accompanied by no significant change in BP but slight increase in HR. Chronic L-NAME administration resulted in depression of NO (84% of control), GSH (90% of control), GSH/GSSG ratio (76% of control), the down-regulation of superoxide dismutase (SOD) (67% of control), GST (74% of control), and GR (90% of control). Plasma CAT and GSH-Px activities, MDA and lactate levels were significantly increased in L-NAME treated rats. The biochemical changes were accompanied by increase in blood pressure and heart rate. Interaction of exercise training and chronic NOS inhibitor treatment resulted in normalization of plasma NO levels, GSH/GSSG ratio, SOD and GST activities, and the up-regulation of, CAT, GSH-Px, and GR activities. The interaction resulted in depletion of plasma MDA levels compared to L-NAME treated group. The biochemical changes were accompanied by decrease in BP and HR compared to L-NAME treated group. The data suggest that the exercise training attenuated the oxidative injury caused by NOS inhibitor by increasing the plasma NO levels, GSH/GSSG ratio and up-regulating the antioxidant enzyme and lowering the BP and HR in the rat.
Husain
Kazim
K
Department of Surgery, Southern Illinois University School of Medicine, 62794, Springfield, IL, USA