Chronic Exercise Preserves Renal Structure and Hemodynamics in Spontaneously Hypertensive Rats

Agarwal, Deepmala; Elks, Carrie M.; Reed, Scott D.; Mariappan, Nithya; Majid, Dewan S. A.; Francis, Joseph

doi:10.1089/ars.2011.3967

Cited by 66 publications

(74 citation statements)

References 60 publications

(64 reference statements)

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“…Indeed, differential expression of ACE and ACE2, Ang II and Ang (1-7), AT1, AT2 and Mas receptors, as well as differential responses to RAS stimulation were observed in vessels, kidney and plasma. 16,27,[34][35][36] One of the most important observations of the present study is that aerobic training promptly downregulates vasoconstrictor and vasodilator RAS axes in vessels of both normotensive and hypertensive animals, with a specific reduction of the vasoconstrictor axis in the renal artery of the SHR. The downregulation was an early response in both strains (significant changes were observed since the first week of training), being more pronounced in hypertensive individuals.…”

Section: Ras Hyperactivity In Hypertension 26-29supporting

confidence: 51%

Downregulation of the Vascular Renin-Angiotensin System by Aerobic Training　– Focus on the Balance Between Vasoconstrictor and Vasodilator Axes –

Silva

Zampieri

Ruggeri

et al. 2015

Circ J

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Although the use of exercise as a therapeutic tool has increased considerably, there is scarce information on the mechanisms conditioning the beneficial effects of training. Previous observations indicate the ability of training to reduce either the activity of the renin-angiotensin system (RAS), oxidative stress and inflammation. 10-12 By evaluating the effects of low-intensity aerobic training on the expression of brain RAS in cardiovascular-controlling areas of spontaneously hypertensive rats (SHR), we observed a prompt and robust training-induced reduction of either angiotensinogen (Aogen) ccumulating experimental evidence has shown that exercise training is an efficient and safe tool to counteract deleterious effects induced by hypertension, coronary artery disease and other cardiovascular diseases. 1-3 Exercise training promotes several cardiovascular adjustments in hypertensive and normotensive individuals, such as remodeling of the heart with a simultaneous stroke volume increase and heart rate (HR) decrease, 1,2,4,5 outward eutrophic remodeling of arteries and arterioles, capillary angiogenesis, and venule neoformation in the exercised muscles. 6-8 Aerobic training also restores impaired endothelial function in hypertensive animals and facilitates artery/arteriole vasodilatation. 2,9 These adaptive mechanisms, by reducing vascular resistance and improving both blood flow and tissue conductance, ameliorate Background: Hyperactivity of the renin-angiotensin system (RAS) and functional deficits in hypertension are reduced after exercise training. We evaluate in arteries, kidney and plasma of hypertensive rats the sequential effects of training on vascular angiotensinogen, Ang II and Ang (1-7) content.

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Section: Ras Hyperactivity In Hypertension 26-29supporting

confidence: 51%

Downregulation of the Vascular Renin-Angiotensin System by Aerobic Training　– Focus on the Balance Between Vasoconstrictor and Vasodilator Axes –

Silva

Zampieri

Ruggeri

et al. 2015

Circ J

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“…These findings indicate a dissociation of changes in blood pressure with changes in renal pathology in these KO mice. Such dissociation between the changes in renal perfusion pressure and in renal morphological injury was not at all unexpected as many previous studies have demonstrated that the reduction in blood pressure by hydralazine or hydrochlorothiazide failed to prevent ANG II-induced renal injury in many animal models of hypertension (1,15,25,36,37). It was also demonstrated that etanercept treatment can markedly reduce renal injury changes without affecting blood pressure in hypertensive rats induced by DOCA salt (11) or ANG II with high-salt intake (12).…”

Section: Discussionmentioning

confidence: 82%

“…However, it is noted that etanercept treatment caused minimal changes in blood pressure in both treated and untreated WT mice with a low dose of ANG II (10 ng/min). As endogenous TNF-␣ production is influenced by the status of oxidative stress (1,29,46,47), which is enhanced during NO deficiency (34), it is likely that the TNF-␣ activity would be greater in KO than in WT mice. Thus, it is expected that the effect of etanercept treatment would be more prominent in KO mice than in WT mice, as seen in the present study.…”

Section: Discussionmentioning

confidence: 99%

Protective role of the endothelial isoform of nitric oxide synthase in ANG II-induced inflammatory responses in the kidney

Whiting

Castillo

Haque

et al. 2013

American Journal of Physiology-Renal Physiology

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Whiting C, Castillo A, Haque MZ, Majid DS. Protective role of the endothelial isoform of nitric oxide synthase in ANG IIinduced inflammatory responses in the kidney. Am J Physiol Renal Physiol 305: F1031-F1041, 2013. First published August 7, 2013 doi:10.1152/ajprenal.00024.2013In the present study, we examine the hypothesis that the nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays a protective role in the development of ANG II-induced hypertension and renal injury by minimizing oxidative stress and the inflammation induced by TNF-␣. Systolic blood pressure (SBP) and renal injury responses to chronic infusions of ANG II (via implanted minipumps) were evaluated for 2 wk in wild-type (WT) and in eNOS knockout mice (KO) cotreated with or without a superoxide (O 2 Ϫ ) scavenger, tempol (400 mg/l in the drinking water), or a TNF-␣ receptor blocker, etanercept (5 mg/kg/day ip). In study 1, when ANG II was given at a dose of 25 ng/min, it increased mean SBP in WT mice (⌬36 Ϯ 3 mmHg; n ϭ 7), and this effect was attenuated in mice pretreated with tempol (⌬24 Ϯ 3 mmHg; n ϭ 6). In KO mice (n ϭ 9), this dose of ANG II resulted in severe renal injury associated with high mortality. To avoid this high mortality in KO, study 2 was conducted with a lower dose of ANG II (10 ng/min) that increased SBP slightly in WT (⌬17 Ϯ 7 mmHg; n ϭ 6) but exaggeratedly in KO (⌬48 Ϯ 12 mmHg, n ϭ 6) associated with severe renal injury. Cotreatment with either tempol (n ϭ 6) or etanercept (n ϭ 6) ameliorated the hypertensive, as well as the renal injury responses in KO compared with WT. These data demonstrate a protective role for eNOS activity in preventing renal inflammatory injury and hypertension induced by chronic increases in ANG II. endothelial nitric oxide synthase activity; tumor necrosis factor-␣; superoxide; angiotensin II; hypertension; renal injury HYPERTENSION IS CONSIDERED to be a low-grade inflammatory condition induced by various proinflammatory cytokines including 43,44). Recent studies have implicated the involvement of TNF-␣ in the development of renal injury in hypertension induced by ANG II (12,43,44). A relationship between the renin-angiotensin system and the production of TNF-␣, and its potential role in regulating cardiovascular function are increasingly evident from the findings of many recent studies (10,18,35,49). TNF-␣ has been implicated in the development of glomerulonephritis (42) as well as saltsensitive hypertension (12) induced by ANG II. It has been observed that chronic ANG II infusion fails to cause hypertensive responses in knockout mice lacking the gene for TNF-␣ (48) or its source, T-lymphocytes (10, 18). ANG II induced up-regulation of the protein expressions of NAD(P)H oxidase enzyme subunit, gp91 phox , and endothelial nitric oxide synthase (eNOS) enzyme in the myocardium was absent in TNF-␣ gene knockout mice (49). These findings suggest an important modulatory role for this cytokine in the nitrosative and oxidative stress mechanisms induced by ANG II.Redox equilibrium is critical f...

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“…Reduced plasma albumin is an independent predictor of renal dysfunction [38] and exercise training (16 weeks at 60% of maximal aerobic velocity) has proven useful at reducing albuminuria (urinary albumin) in SHRs [39]. Nevertheless, a recent review notes a scarcity of data describing the effects of exercise training on plasma albumin in models of CKD [40].…”

Section: Ckd) Is Timelymentioning

confidence: 99%

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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Chronic Exercise Preserves Renal Structure and Hemodynamics in Spontaneously Hypertensive Rats

Abstract: Chronic ExT preserves renal hemodynamics and structure in SHR; these effects are partially mediated by improved redox status and decreased inflammation.

Cited by 66 publications

References 60 publications

Downregulation of the Vascular Renin-Angiotensin System by Aerobic Training　– Focus on the Balance Between Vasoconstrictor and Vasodilator Axes –

Downregulation of the Vascular Renin-Angiotensin System by Aerobic Training　– Focus on the Balance Between Vasoconstrictor and Vasodilator Axes –

Protective role of the endothelial isoform of nitric oxide synthase in ANG II-induced inflammatory responses in the kidney

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

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Chronic Exercise Preserves Renal Structure and Hemodynamics in Spontaneously Hypertensive Rats

Abstract: Chronic ExT preserves renal hemodynamics and structure in SHR; these effects are partially mediated by improved redox status and decreased inflammation.

Cited by 66 publications

References 60 publications

Downregulation of the Vascular Renin-Angiotensin System by Aerobic Training – Focus on the Balance Between Vasoconstrictor and Vasodilator Axes –

Downregulation of the Vascular Renin-Angiotensin System by Aerobic Training – Focus on the Balance Between Vasoconstrictor and Vasodilator Axes –

Protective role of the endothelial isoform of nitric oxide synthase in ANG II-induced inflammatory responses in the kidney

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

Contact Info

Product

Resources

About

Downregulation of the Vascular Renin-Angiotensin System by Aerobic Training　– Focus on the Balance Between Vasoconstrictor and Vasodilator Axes –

Downregulation of the Vascular Renin-Angiotensin System by Aerobic Training　– Focus on the Balance Between Vasoconstrictor and Vasodilator Axes –