Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

Álvarez, María C.; Caldiz, Claudia Irma; Fantinelli, Juliana Catalina; Garciarena, Carolina D.; Cónsole, Gloria M.; Cingolani, Gladys E. Chiappe de; Mosca, Susana M.

doi:10.1291/hypres.31.1465

Cited by 61 publications

(40 citation statements)

References 71 publications

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“…The results of present study confirm the development of oxidative stress in the heart of SHR, characterized by an increase of lipid peroxidation and nucleic acid oxidation according to other evidences regarding the increase of oxidative stress and decreased of catalase, superoxide dismutase and glutathione peroxidase activities in SHR (26). This phenomenon may be related to higher cardiac hypertrophy in SHR compared to WKY rats, indicating that the two effects are associated (20,26).…”

Section: Discussionsupporting

confidence: 89%

Effect of treatment with the antioxidant alpha-lipoic (thioctic) acid on heart and kidney microvasculature in spontaneously hypertensive rats

Tayebati

Tomassoni

Mannelli

et al. 2015

Clinical and Experimental Hypertension

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Endothelial cells represent an important vascular site of signaling and development of damage during ischemia, inflammation and other pathological conditions. Excessive reactive oxygen species production causes pathological activation of endothelium including exposure of cell to adhesion molecules. Intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and platelet-endothelial cell adhesion molecule-1 (PECAM-1) are members of the immunoglobulin super-family which are present on the surface of endothelial cells. These molecules represent important markers of endothelial inflammation. The present study was designed to investigate, with immunochemical and immunohistochemical techniques, the effect of treatment with (+/À)-alpha lipoic (thioctic) acid and its enantiomers on heart and kidney endothelium in spontaneously hypertensive rats (SHR). Arterial hypertension is accompanied by an increased oxidative stress status in the heart characterized by thiobarbituric acid reactive substances (TBARS) and nucleic acid oxidation increase. The higher oxidative stress also modifies adhesion molecules expression. In the heart VCAM-1, which was higher than ICAM-1 and PECAM-1, was increased in SHR. ICAM-1, VCAM-1 and PECAM-1 expression was significantly greater in the renal endothelium of SHR. (+/À)-Alpha lipoic acid and (+)-alpha lipoic acid treatment significantly decreased TBARS levels, the nucleic acid oxidation and prevented adhesion molecules expression in cardiac and renal vascular endothelium. These data suggest that endothelial molecules may be used for studying the mechanisms of vascular injury on target organs of hypertension. The effects observed after treatment with (+)-alpha lipoic acid could open new perspectives for countering heart and kidney microvascular injury which represent a common feature in hypertensive end-organs damage.

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Section: Discussionsupporting

confidence: 89%

Effect of treatment with the antioxidant alpha-lipoic (thioctic) acid on heart and kidney microvasculature in spontaneously hypertensive rats

Tayebati

Tomassoni

Mannelli

et al. 2015

Clinical and Experimental Hypertension

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“…Using the current animals, we previously reported that kidney weight and kidney weight-body weight ratio were significantly lower in HIIT, compared to SED and LIT [19]. Combining our previous results with findings from the current study, we propose that lower kidney weight and kidney weight-body weight ratio in HIIT may have resulted from the structural preservation of renal tissue via enhancements in molecular-level protection by way of up-regulated mRNA expression of renal Sod1 [35,46] and Cat [35,46].…”

Section: Ckd) Is Timelysupporting

confidence: 80%

High intensity interval training favourably affects antioxidant and inflammation mRNA expression in early-stage chronic kidney disease

Tucker

Briskey

Scanlan

et al. 2015

Free Radical Biology and Medicine

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Increased levels of oxidative stress and inflammation have been linked to the progression of chronic kidney disease. To reduce oxidative stress and inflammation related to chronic kidney disease, chronic aerobic exercise is often recommended. Data suggests high intensity interval training may be more beneficial than traditional aerobic exercise. However, appraisals of differing modes of exercise, along with explanations of mechanisms responsible for observed effects, are lacking. This study assessed effects of eight weeks of high intensity interval training (85% VO 2 max), versus low intensity exercise (45-50% VO 2 max) and sedentary behaviour, in an animal model of early-stage chronic kidney disease. We examined kidney-specific mRNA expression of genes related to endogenous antioxidant enzyme activity (glutathione peroxidase 1; Gpx1, superoxide dismutase 1; Sod1, and catalase; Cat) and inflammation (kidney injury molecule 1; Kim1 and tumour necrosis factor receptor super family 1b; Tnfrsf1b), as well as plasma F2-isoprostanes, a marker of lipid peroxidation.Compared to sedentary behaviour, high intensity interval training resulted in increased mRNA expression of Sod1 (p=0.01) and Cat (p<0.001). Compared to low intensity exercise, high intensity interval training resulted in increased mRNA expression of Cat (p<0.001) and Tnfrsf1b (p=0.047). In this study, high intensity interval training was superior to sedentary behaviour and low intensity exercise as high intensity interval training beneficially influenced expression of genes related to endogenous antioxidant enzyme activity and inflammation.

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“…11 However, besides its antihypertensive properties, hydralazine is also an inhibitor of NADH oxidase activity. 36 Given that SHR exhibits increased oxidative stress in the heart, 37 and that recent evidence suggests that arginase activity increases in response to oxidative stress, 38,39 the possibility that hydralazine decreased arginase activity by an antioxidant rather than by a pressure-dependent mechanism cannot be ruled out. However, if true, lung arginase activity, which seems to be independent of blood pressure values, should have been reduced by hydralazine, as oxidative stress is also evident in the lungs of SHRs.…”

Section: Discussionmentioning

confidence: 99%

Misregulation of the arginase pathway in tissues of spontaneously hypertensive rats

Bagnost¹,

Berthelot²,

Alvergnas³

et al. 2009

Hypertens Res

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There is a growing evidence that arginase has a role in the pathophysiology of cardiovascular diseases including hypertension. We recently reported arginase upregulation in aortas from hypertensive spontaneously hypertensive rats (SHRs). The aim of this study was to determine whether arginase abnormalities occur in other tissues of SHR, including the target organs of hypertension. Experiments were conducted on 5-, 10-, 19-and 26-week-old SHRs and Wistar-Kyoto (WKY) rats. Arginase activity and expression were evaluated in heart, kidney, liver, lung and brain tissue extracts. To investigate the role of blood pressure by itself in arginase abnormalities, arginase activity was determined in 10-week-old SHRs previously treated with hydralazine (20 mg kg À1 per day, for 5 weeks). Compared with WKY rats, cardiac arginase activity was higher in hypertensive SHRs aged 10 weeks (+46%, Po0.05), 19 weeks (+29%, Po0.05) and 26 weeks (+23%, NS). Similar results were found in lungs in which arginase activity was increased in SHRs aged 10 weeks (+39%, Po0.05), 19 weeks (+49%, Po0.05) and 26 weeks (+36%, Po0.05) compared with WKY rats. The changes in arginase activity in these tissues were not associated with changes in enzyme expression. The prevention of hypertension by hydralazine blunted the increase in arginase activity in the hearts but not in the lungs. No change in arginase activity/expression was found in the kidney, liver or brain. In conclusion, this study shows that increased arginase activity is not restricted to large vessels in SHRs and suggests that cardiac arginase activity is hemodynamic sensitive.

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Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

Cited by 61 publications

References 71 publications

Effect of treatment with the antioxidant alpha-lipoic (thioctic) acid on heart and kidney microvasculature in spontaneously hypertensive rats

Effect of treatment with the antioxidant alpha-lipoic (thioctic) acid on heart and kidney microvasculature in spontaneously hypertensive rats

High intensity interval training favourably affects antioxidant and inflammation mRNA expression in early-stage chronic kidney disease

Misregulation of the arginase pathway in tissues of spontaneously hypertensive rats

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