Hypertension, the most common cardiovascular disease is the primary reason of stroke coronary artery disease and sudden cardiac death. Many factors are believed to be involved in the pathogenesis of hypertension and complications. Experimental models of human disease are used to study pathophysiolog...
Hypertension, the most common cardiovascular disease is the primary reason of stroke coronary artery disease and sudden cardiac death. Many factors are believed to be involved in the pathogenesis of hypertension and complications. Experimental models of human disease are used to study pathophysiological factors involved in hypertension and assess antihypertensive agents. Today different strains of rats with genetic hypertension are available and in most laboratories, therapeutic studies on hypertension are carried out on these models. As new insights in to the pathogenesis of hypertension are revealed, new models are being developed to produce hypertension in animals. This study reviews experimental models of hypertension, the relevant complications, and approach to ameliorate BP as well as beneficial heath issue. Hypertension is a common chronic condition usually managed by primary care practitioners in different ways. The present study two different experimentally induced hypertensive models and their preventive therapy assessed the characteristics, control and complications of induced hypertensive patients managed at primary healthcare approach. In consideration of above points two different hypertension model and their preventive approach has been evaluated:
In the first study the aim was to prevent metastatic myocardial calcification and hypertension following to CRF in rat. Experimental CRF was induce by subtotal nephrectomy (5/6 nephrectomy) and allocated sham control, nephrectomized nontreatment (NxNT), nephrectomized and treatment with furosemide (NxFuro), nephrectomized and treatment with captopril (NxCap) and nephrectomized and treatment with combinedly furosemide and captopril (NxFuroCap). Oral treatment of furosemide 20 mg/kg, and captopril 0.05 mg/kg was given twice daily until 5 weeks from 2nd week of operation. Hemodynamic, ECG, blood ions, plasma biochemistry, and histopathologycal study were done after five weeks of treatment. The arterial BP in NxNT group was found to be increased significantly compared to control. Furosemide and captorpril separately and combinedly maintained BP to near or below control. Cardiac index in NxNT increased significantly but a nonsignificant difference was observed in treatment groups. High amplitude T-wave, QRS, QT, and QTc interval was recorded significantly higher in NxNT group, which was minimized in the treated groups. Discrete to profuse myocardial metastatic calcification was detected in NxNT and NxCap groups but calcification was disappeared in NxFuro and NxFuroCap groups. Both plasma inorganic phosphate and Ca2+ significantly increased in NxNT, but the difference was not significant in treatment groups. Furosemide alone and in combination with captopril is capable to prevent myocardial calcification, cardiac hypertrophy and hypertension maintaining blood Ca2+ and phosphate levels by slowing the CRF.
In second study the objective was to prevent hypertension and increase of exercise performance in high fructose induced hypertensive rat model. Five groups each of 15, male Sprague-Dawley rats (6 weeks, 125~140 g) were allocated and designated as control group (Con), high fructose-fed sedentary (F), high fructose-fed and exercise (FE), high fructose-fed with 2% taurine supplement and exercise (FET), and high fructose-fed with 2% taurine supplement (FT). BP record significantly (p<0.001) differ from the third week and both invasive and noninvasive measurements significantly (p<0.001) increased and the exercise performance significantly (p<0.001) decreased sedentary (F) group than control. Both exercise and taurine supplementation individually were incapable of preventing the development of hypertension but they kept the pressure to an accessible level in FE and FT groups and the exercise performance in those groups remained near control values. Taurine supplementation along with regular exercise in FET group completely prevented the development of hypertension induced by high fructose as well as the exercise performance increased significantly (p<0.001). The combined effect of taurine supplement and exercise successfully prevented insulin resistance caused by high fructose consumption, augmented the antioxidant system, maintained adequate NO synthesis eventually prevented hypertension and increased exercise performance.
Lifestyle change, including diet, exercise, and stress management, may contribute significantly to lowering of BP. Supplements such as taurine, have been effectively used in the treatment of cardiovascular disease including hypertension.
Hypertension, the most common cardiovascular disease is the primary reason of stroke coronary artery disease and sudden cardiac death. Many factors are believed to be involved in the pathogenesis of hypertension and complications. Experimental models of human disease are used to study pathophysiological factors involved in hypertension and assess antihypertensive agents. Today different strains of rats with genetic hypertension are available and in most laboratories, therapeutic studies on hypertension are carried out on these models. As new insights in to the pathogenesis of hypertension are revealed, new models are being developed to produce hypertension in animals. This study reviews experimental models of hypertension, the relevant complications, and approach to ameliorate BP as well as beneficial heath issue. Hypertension is a common chronic condition usually managed by primary care practitioners in different ways. The present study two different experimentally induced hypertensive models and their preventive therapy assessed the characteristics, control and complications of induced hypertensive patients managed at primary healthcare approach. In consideration of above points two different hypertension model and their preventive approach has been evaluated:
In the first study the aim was to prevent metastatic myocardial calcification and hypertension following to CRF in rat. Experimental CRF was induce by subtotal nephrectomy (5/6 nephrectomy) and allocated sham control, nephrectomized nontreatment (NxNT), nephrectomized and treatment with furosemide (NxFuro), nephrectomized and treatment with captopril (NxCap) and nephrectomized and treatment with combinedly furosemide and captopril (NxFuroCap). Oral treatment of furosemide 20 mg/kg, and captopril 0.05 mg/kg was given twice daily until 5 weeks from 2nd week of operation. Hemodynamic, ECG, blood ions, plasma biochemistry, and histopathologycal study were done after five weeks of treatment. The arterial BP in NxNT group was found to be increased significantly compared to control. Furosemide and captorpril separately and combinedly maintained BP to near or below control. Cardiac index in NxNT increased significantly but a nonsignificant difference was observed in treatment groups. High amplitude T-wave, QRS, QT, and QTc interval was recorded significantly higher in NxNT group, which was minimized in the treated groups. Discrete to profuse myocardial metastatic calcification was detected in NxNT and NxCap groups but calcification was disappeared in NxFuro and NxFuroCap groups. Both plasma inorganic phosphate and Ca2+ significantly increased in NxNT, but the difference was not significant in treatment groups. Furosemide alone and in combination with captopril is capable to prevent myocardial calcification, cardiac hypertrophy and hypertension maintaining blood Ca2+ and phosphate levels by slowing the CRF.
In second study the objective was to prevent hypertension and increase of exercise performance in high fructose induced hypertensive rat model. Five groups each of 15, male Sprague-Dawley rats (6 weeks, 125~140 g) were allocated and designated as control group (Con), high fructose-fed sedentary (F), high fructose-fed and exercise (FE), high fructose-fed with 2% taurine supplement and exercise (FET), and high fructose-fed with 2% taurine supplement (FT). BP record significantly (p<0.001) differ from the third week and both invasive and noninvasive measurements significantly (p<0.001) increased and the exercise performance significantly (p<0.001) decreased sedentary (F) group than control. Both exercise and taurine supplementation individually were incapable of preventing the development of hypertension but they kept the pressure to an accessible level in FE and FT groups and the exercise performance in those groups remained near control values. Taurine supplementation along with regular exercise in FET group completely prevented the development of hypertension induced by high fructose as well as the exercise performance increased significantly (p<0.001). The combined effect of taurine supplement and exercise successfully prevented insulin resistance caused by high fructose consumption, augmented the antioxidant system, maintained adequate NO synthesis eventually prevented hypertension and increased exercise performance.
Lifestyle change, including diet, exercise, and stress management, may contribute significantly to lowering of BP. Supplements such as taurine, have been effectively used in the treatment of cardiovascular disease including hypertension.
주제어
#Hypertension
#Animal model
#Furosemide
#Captopril
#Taurine
#Exercise
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