Effects of angiotensin-converting enzyme inhibition on mitochondrial number in the aging mouse

Ferder, León; Inserra, Felipe; Romano, Luís Alberto; Ercole, Liliana; Pszenny, Viviana

doi:10.1152/ajpcell.1993.265.1.c15

Cited by 87 publications

(62 citation statements)

References 25 publications

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“…We have previously shown [16], that the reduction in the number of mitochondria that occurs with age in mouse hepatocytes and miocardiocytes was prevented by chronic treatment with enalapril. In this paper, we show that enalapril and captopril increase the activities of CuZn-SOD, Mn-SOD, and SeGPx in mouse liver.…”

Section: Discussionmentioning

confidence: 97%

“…In previous work, we found that mice chronically treated with enalapril, a non-sulfhydryl containing ACE inhibitor, showed a reduction in myocardial and glomerular sclerosis and an increase in the number of mitochondria in myocardiocytes and hepatocytes, which was correlated with an increase in their survival, when compared with untreated controls [16]. Considering that it has been widely postulated that ROS are causally involved in the aging process, we hypothesized that enalapril might have altered the prooxidant/antioxidant balance, in favor of the latter, protecting cells from oxidative damage.…”

Section: Introductionmentioning

confidence: 87%

“…The doses were chosen according to Ferder et al [16]. Mice received captopril at a higher dose than enalapril due to the shorter half-life of that compound.…”

Section: Methodsmentioning

confidence: 99%

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Superoxide dismutase and glutathione peroxidase activities are increased by enalapril and captopril in mouse liver

Cavanagh¹,

Inserra²,

Ferder³

et al. 1995

FEBS Letters

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We have characterized the effect of angiotensin converting enzyme (ACE) inhibitors on the activity of CuZn-snperoxide dismntase (CuZn-SOD), Mn-snperoxide dismutase (Mn-SOD), catalase, and selenium-dependent glutathione peroxidase (Se-GPx). CF1 mice (4-month-old females) were administered water containing enalapril (20 rag/l) or captopril (50 rag/I), during 4 to 11 weeks. After 11 weeks, enalapril treatment caused an increase in the activity of CuZn-SOD, Mn-SOD and Se-GPx, from 19 -+ 4 to 46 +-7, 2.1 -+ 0.2 to 3.8 --0.2 units/mg protein and 27--3 to 54--3 milliunits/mg protein, respectively. After 11 weeks, captopril treatment increased the activities (P < 0.05) of CuZn-SOD, MnSOD and Se-GPx to 35 -+ 4, 2.9 --0.2 nnitslmg protein, and 38 + 2 millianits/mg protein, respectively. Catalase activity was not affected by the treatments. These results suggest that ACE inhibitors may protect cell components from oxidative damage by increasing the enzymatic antioxidant defenses.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 87%

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Superoxide dismutase and glutathione peroxidase activities are increased by enalapril and captopril in mouse liver

Cavanagh¹,

Inserra²,

Ferder³

et al. 1995

FEBS Letters

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“…17 In the same study it was also demonstrated that enalapril treatment prevented glomerular enlargement and mesangial expansion. 17 In addition to hyperfiltration, it has recently been shown that glomerular enlargement and mesangial expansion are major factors in the development of glomerulosclerosis.…”

Section: Discussionmentioning

confidence: 86%

“…Furthermore, we showed that the decrease in glomerular and myocardial sclerosis in those animals was related to an increase in the number of hepatic and cardiac mitochondria. 17 These findings suggest a relation between the deletion of the mitochondrial genome and aging. In the present study we provide evidence that natural aging is associated with intraglomerular expression of a-SM actin and that treatment with enalapril from early life prevents the early changes associated with glomerular injury and the expression of a-SM actin in the glomerulus.…”

mentioning

confidence: 89%

Intraglomerular expression of alpha-smooth muscle actin in aging mice.

Romano¹,

Ferder²,

Inserra³

et al. 1994

Hypertension

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To determine whether chronic treatment with enalapril initiated early in life prevents glomerular injury secondary to normal aging, CF1 mice received enalapril (20 mg/L, n=10) or nifedipine (40 mg/L, n=10) in their drinking water from the time of weaning to 12 months of life. Control mice (n=10) received tap water ad libitum. Immunocytochemical detection of renin confirmed that angiotensin-converting enzyme inhibition resulted in recruitment of renin-containing cells along the preglomerular vessels. Morphometric analysis of glomeruli included assessment of glomerular diameter and the percentage of mesangial area per glomerulus. Glomerular diameter and mesangial area were higher in control mice (99.7±0.5 fim, 12.7±0.3%) than in enalapril-treated mice (88±0.8 fim, 8.6±0.6%) (P<.05). Glomerular diameter and mesangial area in the nifedipine-treated group (99.1 ±0.9 fim,

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Prognostic impact of Clinical Frailty Scale in patients with heart failure with preserved ejection fraction

et al. 2021

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Aims Frailty is associated with prognosis of cardiovascular diseases. However, the significance of frailty in patients with heart failure with preserved ejection fraction (HFpEF) remains to be elucidated. The purpose of this study was to examine the prognostic significance of the Clinical Frailty Scale (CFS) in real-world patients with HFpEF using data from a prospective multicentre observational study of patients with HFpEF (PURSUIT-HFpEF study). Method and ResultsWe classified 842 patients with HFpEF enrolled in the PURSUIT-HFpEF study into two groups using CFS. The registry enrolled patients hospitalized with a diagnosis of decompensated heart failure. Median age was 82 [interquartile range: 77, 87], and 45% of the patients were male. Of 842 patients, 406 were classified as high CFS (CFS ≥ 4, 48%) and 436 as low CFS (CFS ≤ 3, 52%). The primary endpoint was the composite of all-cause mortality and heart failure admission. Secondary endpoints were all-cause mortality and heart failure admission. Patients with high CFS were older (85 vs. 79 years, P < 0.001), predominantly female (65% vs. 46%, P < 0.001) and more likely to have New York Heart Association (NYHA) ≥ 2 (75% vs. 53%, P < 0.001) and a higher level of NT-proBNP (1360 vs 838 pg/mL, P < 0.001) than those with low CFS. Patients with high CFS had a significantly greater risk of composite endpoint (Kaplan-Meier estimated 1-year event rate 39% vs. 23%, log-rank P < 0.001), all-cause mortality (Kaplan-Meier estimated 1-year event rate 17% vs. 7%, log-rank P < 0.001) and heart failure admission (Kaplan-Meier estimated 1-year event rate 28% vs. 19%, log-rank P = 0.002) than those with low CFS. Multivariable Cox regression analysis revealed that high CFS was significantly associated with composite endpoint (adjusted HR 1.92, 95% CI 1.35-2.73, P < 0.001), all-cause mortality (adjusted HR 2.54, 95% CI 1.39-4.66, P = 0.003) and heart failure admission (adjusted HR 1.55, 95% CI 1.03-2.32, P = 0.035) even after adjustment for covariates. Moreover, change in CFS grade was also significantly associated with composite endpoint (adjusted HR 1.23, 95% CI 1.11-1.36, P < 0.001), all-cause mortality (adjusted HR 1.32, 95% CI 1.13-1.55, P = 0.001) and heart failure admission (adjusted HR 1.15, 95% CI 1.02-1.30, P = 0.021). Conclusions Frailty assessed by the CFS was associated with poor prognosis in patients with HFpEF.

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Effects of angiotensin-converting enzyme inhibition on mitochondrial number in the aging mouse

Cited by 87 publications

References 25 publications

Superoxide dismutase and glutathione peroxidase activities are increased by enalapril and captopril in mouse liver

Superoxide dismutase and glutathione peroxidase activities are increased by enalapril and captopril in mouse liver

Intraglomerular expression of alpha-smooth muscle actin in aging mice.

Prognostic impact of Clinical Frailty Scale in patients with heart failure with preserved ejection fraction

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