Study On The Mechanism Of Hypertension And Deep Venous Thrombosis Caused By Chronic Stress

Part 1 Role of the renal sympathetic nerve system and renin-angiotensin system in chronic stress-induced hypertension in ratsObjective:In the study of prevention and treatment of hypertension, it was discovered that a long-term chronic stress can seriously affect people’s health, so that the body will be in a sub-healthy condition, and even suffer the stress-induced hypertension. Studies have demonstrated that renal sympathetic nervous system(RSNS) and the renin-angiotensin system(RAS) play a key role in the pathogenesis of renal hypertension and spontaneous hypertension. The pathogenesis of stress induced hypertension was less reported at home and abroad before. This experiment will focus on exploring the role of the renin-angiotensin system and the sympathetic nervous system in stress-induced renal hypertensive.Methods:Male Sprague-Dawley rats were divided into six groups: control, chronic foot shock, RSNS denervation, denervation plus foot shock, Captopril(angiotensin I converting enzyme inhibitor, ACE inhibitor) plus foot shock, and Tempol(superoxide dismutase mimetic) plus foot shock. Rats received foot shock for 14 days. The mean arterial pressure was measured. The concentrations of stress hormone–corticosterone in plasma and norepinephrine(NE) in kidney were measured; We measured the level of peripheral RAS: the quantity of renin and angiotensin II(Ang II) in plasma; We measured the level of central RAS: the m RNA and protein levels of RAS component in the cerebral cortex and hypothalamus; We quantified the concentrations of thiobarbituric acid reactive substances(TBARS), the activities of superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px).Results:1. The two weeks foot shock treatment significantly increased systolic blood pressure, it was significantly supressed by denervation or treatment with Tempol or Captopril.2. The two weeks foot shock treatment significantly increased the plasma concentrations of corticosterone and norepinephrine concentrations of kidney, the rats were in stress, and these were significantly supressed by denervation or treatment with Tempol or Captopril.3. The concentrations of rennin and Ang II in plasma were significantly heightened after the two weeks foot shock treatment, and these were significantly supressed by denervation or treatment with Tempol or Captopril.4. The angiotensinogen, ACE1, ACE2 and AT1 a m RNA and protein expression in the cerebral cortex and hypothalamus were significantly increased after the two weeks foot shock treatment, and these were also partially restored by denervation or treatment with Tempol or Captopril.5. The rat plasma TBARS levels were significantly increased while plasma SOD,GSH-Px activities were significantly reduced after the two weeks foot shock treatment,the oxidative/antioxidant system imbalanced, and the oxidative level increased, this phenomenon was not occurred in the denervation or treatment with Tempol or Captopril groups.Conclusions:RSNS, RAS and oxidative stress reciprocally potentiate to play important roles in the development of foot shock-induced hypertension.Part 2 Role of renal sympathetic nerve system and oxidative stress in chronic stress-induced deep venous thrombosis in ratsObjective:Deep vein thrombosis(DVT) refers to abnormal blood coagulation in the deep vein lumen, it is a common and multiple cardiovascular disease, in recent years, the prevalence and diagnosis rate of DVT showing a trend of increasing year by year in our country, so it is significative to investigate its pathogenesis for the DVT prevention and treatment. This experiment will focus on exploring the pathogenesis of foot shock-induced DVT.Methods:Male Sprague–Dawley rats were divided into six groups: control, chronic foot shock, denervation plus foot shock and Tempol(superoxide dismutase mimetic) plus foot shock. The concentrations of stress hormone–corticosterone in plasma and norepinephrine(NE) in kidney were measured. We quantified the concentrations of thiobarbituric acid reactive substances(TBARS), the activities of superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px). Prothrombin time(PT), activated partial thromboplastin time(APPT) and thrombin time(TT) were measured by semi-automatic blood coagμLation analyzer. ADP and collagen induced platelet aggregation were measured through platelet aggregation instrument. The deep vein thrombosis(DVT)model was made and the weight of the thrombus was measured.Results:1. The two weeks foot shock treatment significantly increased the plasma concentrations of corticosterone and norepinephrine concentrations of kidney, the rats were in stress, and these were significantly supressed by denervation or treatment with Tempol.2. The rat plasma TBARS levels were significantly increased while plasma SOD,GSH-Px activities were significantly reduced after the two weeks foot shock treatment,the oxidative/antioxidant system imbalanced, and the oxidative level increased, thisphenomenon was not occurred in the denervation or treatment with Tempol groups.3. The TT was remarkably lifted after the two weeks foot shock treatment, and it was significantly supressed by denervation or treatment with Tempol.4. ADP or collagen induced platelet aggregation of foot shock group were significantly higher than control group, and it was significantly supressed by denervation or treatment with Tempol.5. The weight of thrombus in foot shock group was increased compared with control group, both of renal sympathetic denervation and Tempol treatments reduced the weight of the thrombus compared with foot shock group.Conclusions:Foot shock of rats enhanced blood coagμLation system through renal sympathetic nerve system activation and increase of oxidative stress.