Enalapril and captopril enhance glutathione-dependent  antioxidant defenses in mouse tissues

Cavanagh, Elena M.V. de; Inserra, Felipe; Ferder, León; Fraga, César G.

doi:10.1152/ajpregu.2000.278.3.r572

Cited by 127 publications

(95 citation statements)

References 29 publications

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“…Moreover, the ACEI-induced increase in GPx activity is significantly blunted by coadministration of the B2R antagonist. Such stimulation or protection of anti-oxidant systems by ACEI inhibitors has been previously documented in various tissues in aging mice and rats (9,11,13), in hemodialysis patients (10), and in diabetic rats (12).…”

Section: Discussionmentioning

confidence: 65%

ACE inhibitor reduces growth factor receptor expression and signaling but also albuminuria through B2-kinin glomerular receptor activation in diabetic rats

Allard¹,

Buléon²,

Cellier³

et al. 2007

American Journal of Physiology-Renal Physiology

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Tack I, Girolami J-P. ACE inhibitor reduces growth factor receptor expression and signaling but also albuminuria through B2-kinin glomerular receptor activation in diabetic rats. Am J Physiol Renal Physiol 293: F1083-F1092, 2007. First published June 27, 2007; doi:10.1152/ajprenal.00401.2006 is associated with increased oxidative stress, overexpression and activation of growth factor receptors, including those for transforming growth factor-␤1 (TGF-␤-RII), platelet-derived growth factor (PDGF-R), and insulin-like growth factor (IGF1-R). These pathways are believed to represent pathophysiological determinants of DN. Beyond perfect glycemic control, angiotensin-converting enzyme inhibitors (ACEI) are the most efficient treatment to delay glomerulosclerosis. Since their mechanisms of action remain uncertain, we investigated the effect of ACEI on the glomerular expression of these growth factor pathways in a model of streptozotocin-induced diabetes in rats. The early phase of diabetes was found to be associated with an increase in glomerular expression of IGF1-R, PDGF-R, and TGF-␤-RII and activation of IRS1, Erk 1/2, and Smad 2/3. These changes were significantly reduced by ACEI treatment. Furthermore, ACEI stimulated glutathione peroxidase activity, suggesting a protective role against oxidative stress. ACEI decreased ANG II production but also increased bradykinin bioavailability by reducing its degradation. Thus the involvement of the bradykinin pathway was investigated using coadministration of HOE-140, a highly specific nonpeptidic B2-kinin receptor antagonist. Almost all the previously described effects of ACEI were abolished by HOE-140, as was the increase in glutathione peroxidase activity. Moreover, the well-established ability of ACEI to reduce albuminuria was also prevented by HOE-140. Taken together, these data demonstrate that, in the early phase of diabetes, ACEI reverse glomerular overexpression and activation of some critical growth factor pathways and increase protection against oxidative stress and that these effects involve B2-kinin receptor activation.angiotensin-converting enzyme inhibitor; oxidative stress; glutathione peroxidase activity; diabetes DIABETIC NEPHROPATHY (DN) causes the majority of end-stage renal diseases throughout the world (54). It was initially believed that elevated blood glucose was the major cause of renal damage in both type 1 and 2 diabetes. However, several clinical studies have demonstrated that strict glycemic control is not sufficient to prevent the progression of renal dysfunction and the development of glomerular lesions. The mechanisms underlying the progression of diabetic kidney disease are intricate and still not completely understood. Among the many pathophysiological mechanisms possible, several growth factors and cytokines have been put forward to account for the onset of DN. This is particularly the case for the paracrine expression of insulin-like growth factor-1 (IGF-1), transforming growth factor-␤ (TGF-␤) (20), and platelet-derived growth factor (PDG...

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Section: Discussionmentioning

confidence: 65%

ACE inhibitor reduces growth factor receptor expression and signaling but also albuminuria through B2-kinin glomerular receptor activation in diabetic rats

Allard¹,

Buléon²,

Cellier³

et al. 2007

American Journal of Physiology-Renal Physiology

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“…Another group 41 investigated the vascular effects of ARB in hypertensive patients and found that compared with control, ARB significantly reduced plasma MDA level. Couple of researchers 42 examined the effect of AT 1 receptor blocker on atherosclerosis and found that MDA was reduced compared to control. Inhibition of lipid peroxidative effect in this study caused by enalapril and valsartan was 39.34% and 25.41% respectively.…”

Section: Discussionmentioning

confidence: 99%

Modulation of oxidative stress by enalapril and valsartan in adrenaline treated rats: a comparative study

Huda¹,

Akhter

2014

Bangladesh Med Res Counc Bull

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Angiotensin (Ang II) II is known to promote oxidative stress in acute myocardial infarction (AMI). Inhibition of renin angiotensin system (RAS) or blockade of Ang II receptors may therefore be effective in reducing oxidative stress during AMI. The study evaluates and compares the protective effect of Angiotensin Converting Enzyme (ACE) inhibitor and AT 1 receptor blocker in adrenaline induced oxidative stress in rats. Rats were treated with two successive injections of adrenaline subcutaneously at a dose of 2 mg/kg administered 24 hours apart. In other two groups of rats enalapril (30 mg/kg) or valsartan (30 mg/kg) were given orally once daily through intragastric tube for 2 weeks and then two injections of adrenaline were administered 24 hours apart. Serum Aspertate Transaminase (AST), plasma Malonde Aldehyde (MDA), erythrocyte GSH and serum vitamin E levels were measured 24 hours after the 2 nd injection of adrenaline in all the groups. Administration of adrenaline caused significant increase (p<0.001) in serum AST and plasma MDA levels and decrease (p<0.001) in erythrocyte GSH and serum vitamin E levels. Pre-treatment of enalapril or valsartan for 14 days reduced (p<0.001) serum AST and plasma MDA levels and increased the concentration of erythrocyte GSH in enalapril pre-treated group (p<0.01) and in valsartan pre-treated group (p<0.05). Pre-treatment of enalapril or valsartan also increased (p<0.01) serum vitamin E levels in adrenaline treated rats. However, no significant difference was noted between the effect of enalapril and valsartan on serum AST, plasma MDA, erythrocyte GSH and serum vitamin E levels. It may be concluded that both enalapril and valsartan offered cardioprotection in adrenaline induced oxidative stress, but the protection afforded by valsartan was not superior to enalapril.

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“…Experimental findings that chronic treatment with ACEIs or ARBs attenuates most of the deleterious effects due to aging in the kidney (Inserra et al, 1996;Ferder et al, 2002) indicate the contribution of the RAS to age-dependent changes in renal function and structure. Further studies indicate that the beneficial effects of Ang II blockade on kidney aging are mediated through their antioxidative actions (Ferder et al, 1993;de Cavanagh et al, 1997de Cavanagh et al, , 2000. However, studies also indicate that aging is associated with reduced plasma renin activity and unchanged plasma angiotensinogen or ACE levels (Weidmann et al, 1975;Corman and Michel, 1986).…”

Section: Renal Development and Agingmentioning

confidence: 99%

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

et al. 2007

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Enalapril and captopril enhance glutathione-dependent antioxidant defenses in mouse tissues

Cited by 127 publications

References 29 publications

ACE inhibitor reduces growth factor receptor expression and signaling but also albuminuria through B2-kinin glomerular receptor activation in diabetic rats

ACE inhibitor reduces growth factor receptor expression and signaling but also albuminuria through B2-kinin glomerular receptor activation in diabetic rats

Modulation of oxidative stress by enalapril and valsartan in adrenaline treated rats: a comparative study

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

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