scholarly journals Geniposide from Gardenia jasminoides var. radicans Makino Attenuates Myocardial Injury in Spontaneously Hypertensive Rats via Regulating Apoptotic and Energy Metabolism Signalling Pathway

2021 ◽  
Vol Volume 15 ◽  
pp. 949-962
Author(s):  
Ying Hou ◽  
Peipei Yuan ◽  
Yang Fu ◽  
Qi Zhang ◽  
Liyuan Gao ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Spontaneously Hypertensive Rats ◽  
Myocardial Injury ◽  
Signalling Pathway ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Gardenia Jasminoides

Age changes in enzymes of neuronal and microvascular energy metabolism in the brain of spontaneously hypertensive rats

1990 ◽  
Vol 109 (5) ◽  
pp. 682-685
Author(s):  
V. A. Sorokoumov ◽  
Yu. Ya. Kislyakov ◽  
E. L. Pugacheva ◽  
E. R. Barantsevich ◽  
V. A. Grantyn'
Keyword(s):  
Energy Metabolism ◽  
Spontaneously Hypertensive Rats ◽  
Age Changes ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
The Brain

scholarly journals Effects of Aerobic Exercise on Energy Metabolism in the Hypertensive Rat Heart

2001 ◽  
Vol 81 (4) ◽  
pp. 1006-1017 ◽  
Author(s):  
Tanya L Kinney LaPier ◽  
Kenneth J Rodnick
Keyword(s):  
Blood Pressure ◽  
Energy Metabolism ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Spontaneously Hypertensive Rats ◽  
Aerobic Exercise Training ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cardiac Energy Metabolism ◽  
Cardiac Energy

AbstractBackground and Purpose. In order to explore the possible effects of physical therapy interventions on patients with hypertension, we evaluated the effects of aerobic exercise training on myocardial energy metabolism in an animal model of hypertension. Subjects. We used 36 female spontaneously hypertensive rats (rats with genetically induced hypertension) and 12 normotensive Wistar-Kyoto rats. Methods. The normotensive rats were sedentary and formed the CONsed group. The spontaneously hypertensive rats were randomly divided into 3 experimental groups (12 rats per group). Hypertensive rats that were sedentary formed the HTNsed group, those that received 8 weeks of exercise training formed the HTN×8 group, and those that received 16 weeks of exercise training formed the HTN×16 group. We measured systolic blood pressure, heart wet weight, maximal activities of cardiac energy metabolism enzymes, glucose transporter content, and total concentrations of protein, glycogen, and triglyceride. Results. Systolic blood pressure was greater than 200 mm Hg in the CONsed group at the time of testing. Exercise training modestly (∼11–18 mm Hg) lowered blood pressure in the HTN×8 and HTN×16 groups. Fatty acid enzyme activity was greater in the CONsed group than in the HTNsed and HTN×8 groups, but activity was roughly equivalent between the CONsed group and the HTN×16 group. Glucose enzyme activity was greater in the HTN×16 group than in the CONsed group and the HTNsed group. Intracellular glycogen concentration was greater in the HTN×8 group than in the HTNsed group. Discussion and Conclusion. Results of this study suggest that aerobic exercise training may help to normalize cardiac energy metabolism in mammals with hypertension.

Reduction of asymmetric dimethylarginine involved in the cardioprotective effect of losartan in spontaneously hypertensive rats

2007 ◽  
Vol 85 (8) ◽  
pp. 783-789 ◽  
Author(s):  
Dai Li ◽  
Ke Xia ◽  
Nian-Sheng Li ◽  
Dan Luo ◽  
Shan Wang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Creatine Kinase ◽  
Cardiac Function ◽  
Spontaneously Hypertensive Rats ◽  
Myocardial Injury ◽  
Asymmetric Dimethylarginine ◽  
Left Ventricular ◽  
Ischemia And Reperfusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Previous studies have indicated that nitric oxide synthase (NOS) inhibitors can induce an increase of blood pressure and exacerbate myocardial injury induced by ischemia and reperfusion, whereas angiotensin II receptor antagonists protect the myocardium against injury induced by ischemia and reperfusion. Isolated hearts from male spontaneously hypertensive rats (SHR) or male Wistar-Kyoto rats (WKY) were subjected to 20 min global ischemia and 30 min reperfusion. Heart rate, coronary flow, left ventricular pressure, and its first derivatives (±dP/dtmax) were recorded, and serum concentrations of asymmetric dimethylarginine (ADMA) and NO and the release of creatine kinase in coronary effluent were measured. The level of ADMA was significantly increased and the concentration of NO was decreased in SHR. Ischemia and reperfusion significantly inhibited the recovery of cardiac function and increased the release of creatine kinase, and ischemia and reperfusion-induced myocardial injury in SHR was aggravated compared with WKY. Vasodilation responses to acetylcholine of aortic rings were decreased in SHR. Treatment with losartan (30 mg/kg) for 14 days significantly lowered blood pressure, elevated the plasma level of NO, and decreased the plasma concentration of ADMA in SHR. Treatment with losartan significantly improved endothelium-dependent relaxation and cardiac function during ischemia and reperfusion in SHR. Exogenous ADMA also aggravated myocardial injury induced by ischemia and reperfusion in isolated perfused heart of WKY, as shown by increasing creatine kinase release and decreasing cardiac function. The present results suggest that the protective effect of losartan on myocardial injury induced by ischemia and reperfusion is related to the reduction of ADMA levels.

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