| OBJECTIVES: Hypertension is the main risk factor for cardiovascular and cerebrovascular disease with high incidence of disease and mortality in China. Recently research indicates that platelets play an important part in hypertension and its complication of thrombosis. The change of platelet function is related to the occurrence, development and transformation of these diseases. Platelets possess the L-Arg/Nitric Oxide pathway via constitutive nitric oxide synthase, which has been identified in human platelets. Platelet-derived nitric oxide (PDNO) plays functional role in the inhibition of not only platelet aggregation, but also platelet recruitment. Previous studies have documented that platelet L-Arg/NO pathway and PGI2-TXB2 balance was impaired in hypertensive. Decreasing of PDNO and PGI2 production induces the enhancement of platelet aggregation, which then results in thrombosis in hypertensive. As an effective treatment for prevention of thrombosis in hypertensive, moderate exercise training, has been applied extensively. However, little is known about the functional mechanism of exercise on platelets L-Arg/NO pathway and the balance between PGI2 and TXB2 in hypertension. Accordingly, this study is undertaken to determine whether exercise affects platelets L-Arg/NO pathway or the balance between PGI2 and TXB2, and to discuss the possible mechanism of change of platelet function and thrombosis induced by exercise, which provides theoretical basis for application of exercise in prevention of thrombosis in hypertensive.DESIGNS AND METHODS: male spontaneously hypertensive rats (SHR) were divided into 2 groups randomly: control group (8 SHR) and exercise group (10 SHR). SHR were exercised on a swimming (5 times/wk) at moderate intensity(60min/times) for a period of 10 wk. Resting blood pressures and body weight were obtained fortnightly during exercise training periods. After the exercise period, the ADP(2umol/L) induced platelet aggregation (1 min 5min and maximal platelet aggregation) , the concentration of PDNO, platelet NOS activity and intraplatelet levels of cGMP were measured, simultaneously, plasma 6-Keto-PGF1a and TXB2 concentration were also measured.RESULTS: (1) Compared with the control group, the extent the body weight ofexercise group SHR puts on decreases followed by ages. The body weight and resting blood pressure were significantly decreased by 4.8% (P<0.05) and 13.6% (P<0.01) respectively after 10-week swimming exercise in exercise group SHR. The resting blood pressure in control group SHR was increased by 7.9% (P<0.01) while it was significantly decreased by 6.2% in exercise group (P<0.01) compared with that of pre-exercise. It shows that moderate exercise may have an important role in inhibiting the increase of SHR body weight and blood pressure.(2) Compared with the control group, the ADP induced PAG(l), PAG(5) and PAG(M) were significantly decreased (P<0.05, P<0.01 and P<0.01 respectively) in exercise group SHR. It is supported that exercise can decrease SHR platelet aggregation and sensitivity to agonist and this may inhibit the formation of platelet thrombus.(3) Compared with the control group, the concentration of PDNO, the activity of NOS in platelet and intraplatelet levels of cGMP in exercise group were significantly increased by 9.6% (P<0.05) , 23.5%(P<0.01) and 42.9%(P<0.01) respectively. The concentration of plasma 6-Keto-PGFla was significantly increased (P<0.05) while TXB2 was significantly decreased(P<0.01) and PGI2/TXB2-ratio was also significantly increased after 10-week swimming exercise. It indicates that 10-week swimming exercise can improve platelet L-arginine/Nitric Oxide pathway and the balance between PGI2 and TXB2 to inhibit platelet aggregation and thrombosis.CONCLUSION: This study implies that long-term regular moderate exercise training can inhibit the increase of blood pressure as well as thrombosis in hypertension. The mechanism of Training-induced preventing thrombosis may be mediated by improving platelet L-Arg/NO pathway and the balance betwe... |
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