Angiotensin I-Converting Enzyme Activity in Rats with Carbon Tetrachloride-Induced Acute Renal Failure

Pedraza‐Chaverrí, José; Cruz, Cristino; Hernández-Pando, Rogelio; Santana, Thalia S.; Arévalo, Ana Elena; González, L.; Tapia, Edilia; Peña, José Carlos; Panduro, Arturo

doi:10.3109/08860229309065567

Cited by 9 publications

(5 citation statements)

References 23 publications

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“…Urinary volume increased on days 1-3 and returned to control values on day 7. These data are in close agreement with previously reported values in this experimental model (Pedraza-Chaverri et al 1993).…”

Section: Discussionsupporting

confidence: 95%

“…In the present study, male Wistar rats weighing 200-220 g were used. Carbon tetrachloride was administered by gavage to 80 rats as a single dose (2.5 mL/ kg) mixed with an equal volume of corn oil (Pedraza-Chaverri et al 1993). Control animals ( n = 17) received the same volume of the vehicle.…”

Section: Experimental Designmentioning

confidence: 99%

“…Control animals ( n = 17) received the same volume of the vehicle. The animals were maintained in metabolic cages and killed by decapitation on days 1, 2, 3 and 7 after CCL administration (Pedraza-Chaverri et al 1993). Urine volume was collected during the 24 h before decapitation.…”

Section: Experimental Designmentioning

confidence: 99%

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Circulating Levels of Active, Total and Inactive Renin (Prorenin), Angiotensin I and Angiotensinogen in Carbon Tetrachloride‐treated Rats

Cruz

Ibarra-Rubio

Pedraza‐Chaverrí

1993

Clin Exp Pharma Physio

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1. Plasma renin activity (PRA), plasma angiotensin I concentration (ANG I), plasma angiotensinogen concentration (PAC) and the plasma levels of active, total and inactive renin (prorenin) were measured in rats with carbon tetrachloride (CCl4)-induced acute renal failure. Rats were treated with a single oral dose of CCl4 (2.5 mL/kg) and killed 1, 2, 3 and 7 days later. 2. On days 1-3 PRA, ANG I and PAC decreased and increased on day 7. Active renin fell on days 2 and 3, total renin (trypsin treatment) augmented on day 1 and diminished on day 3, prorenin and per cent prorenin increased on days 1 and 2. Angiotensin I concentration paralleled PRA and PAC. The CCl4-induced decrease in PRA was secondary to the fall in active renin and in PAC. Total renin augmented as a consequence of the elevation of prorenin. Renal function, evaluated by serum urea, serum creatinine and creatinine clearance, decreased on days 1 and 2 when PRA was low and plasma prorenin was high. 3. These data do not support the involvement of the circulating active renin-angiotensin system (RAS) in the pathophysiology of acute renal failure induced by CCl4, however, increased prorenin levels were associated with the decrease in renal function.

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Section: Discussionsupporting

confidence: 95%

Section: Experimental Designmentioning

confidence: 99%

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Circulating Levels of Active, Total and Inactive Renin (Prorenin), Angiotensin I and Angiotensinogen in Carbon Tetrachloride‐treated Rats

Cruz

Ibarra-Rubio

Pedraza‐Chaverrí

1993

Clin Exp Pharma Physio

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“…Sections of 1 lm were stained with toluidine blue and examined with a light microscopy to select representative areas from which ultrathin sections were obtained [32]. These sections were contrasted with uranyl acetate and lead citrate and examined with a FEI Tecnai TM G2 transmission electron microscope (Hillsboro, OR, USA).…”

Section: Electron Microscopy Studies Of Mitochondria In Renal Tissuementioning

confidence: 99%

C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress

et al. 2015

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The potential of C-phycocyanin (C-PC) to prevent cisplatin (CP)-induced kidney mitochondrial dysfunction was determined in CD-1 male mice. The CP-induced mitochondrial dysfunction was characterized by ultrastructural abnormalities and by decrease in the following parameters in isolated kidney mitochondria: adenosine diphosphate (ADP)-induced oxygen consumption (state 3), respiratory control ratio, ADP/oxygen (ADP/O) ratio, adenosine triphosphate synthesis, membrane potential, calcium retention, glutathione (GSH) content, and activity of respiratory complex I, aconitase, catalase, and GSH peroxidase. These mitochondria also showed increase in hydrogen peroxide production, malondialdehyde, and 3-nitrotyrosine protein adducts content. The above-described changes, as well as CP-induced nephrotoxicity, were attenuated in mice pretreated with a single injection of C-PC. Our data suggest that the attenuation of mitochondrial abnormalities is involved in the protective effect of C-PC against CP-induced nephrotoxicity. This is the first demonstration that C-PC pretreatment prevents CP-induced mitochondrial dysfunction in mice.

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“…In rat acute renal failure caused by mercuric chloride, potassium dichromate, and uranyl nitrate increased serum ACE activity significantly [16][17][18]. In puromycin aminonuleoside (PAN)-nephrotic rats high serum ACE activity was observed [19][20][21].…”

Section: Discussionmentioning

confidence: 99%

Gentamicin Reduces Serum ACE Activity in Patients with Normal Kidney Function

Ziai

Mahmoudian

2002

Am J Nephrol

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Aims: We evaluated serum angiotensin-converting enzyme (ACE) as an indicator of gentamicin toxicity and compared it with N-acetyl-β-D-glucosaminidase (NAG) and creatinine. Methods: 20 bone fracture in-patients receiving gentamicin 80 mg TDS for 3 days. Subjects had normal kidney function and had no history or sign of hypertension. Serum and urine samples were collected before and 3 days after drug administration. Samples analyzed for ACE, NAG, BUN, creatinine, sodium, and potassium. Results: Our results showed that urine NAG activity increased significantly at the 3rd day. Serum creatinine level and glomerular filtration rate (GFR) while still at a normal range showed slight but significant changes at this time. This may indicate some renal damage. Serum ACE activity decreased significantly at the 3rd day. Conclusion: These results indicate serum ACE can be used as a good indicator of renal damage in patients receiving gentamicin.

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Angiotensin I-Converting Enzyme Activity in Rats with Carbon Tetrachloride-Induced Acute Renal Failure

Cited by 9 publications

References 23 publications

Circulating Levels of Active, Total and Inactive Renin (Prorenin), Angiotensin I and Angiotensinogen in Carbon Tetrachloride‐treated Rats

Circulating Levels of Active, Total and Inactive Renin (Prorenin), Angiotensin I and Angiotensinogen in Carbon Tetrachloride‐treated Rats

C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress

Gentamicin Reduces Serum ACE Activity in Patients with Normal Kidney Function

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