Evaluation of the use of captopril on peritoneal fibrosis induced in rats by the use of glucose solution 4.25%

Schuinski, Adriana Fatima Menegat; Baroni, Gilberto; Filho, Roberto F. Pecoits; Meyer, Fernando; Cerqueira, Marina Lindstrom Wittica; Silva, Maria Angélica Alexandre da; Carvalho, Viviane de Souza Correia de

doi:10.5935/0101-2800.20130046

Cited by 2 publications

(1 citation statement)

References 13 publications

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“…In a subsequent study using the same model, these authors found that the AT1R antagonist valsartan was equal to the ACE inhibitor lisinopril in mitigating peritoneal injury caused by glucose-containing PD fluid (19). In a similar study from another laboratory, PD fluid containing 4.25% glucose was injected into the peritoneal space of rats with normal renal function daily for 3 or 7 weeks, and the ACE inhibitor captopril at 30 mg/kg/d was administered by gavage each day to half of the animals (20). There were trends toward less peritoneal thickness, less cellularity, and less collagen expression in the captopril group, especially in the parietal peritoneum, but statistical significance was not reached.…”

Section: Peritoneal Dialysismentioning

confidence: 99%

Angiotensin II receptors and peritoneal dialysis-induced peritoneal fibrosis

Morinelli

Luttrell

Strungs

et al. 2016

The International Journal of Biochemistry & Cell Biology

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The vasoactive hormone angiotensin II initiates its major hemodynamic effects through interaction with AT1 receptors, a member of the class of G protein-coupled receptors. Acting through its AT1R, angiotensin II regulates blood pressure and renal salt and water balance. Recent evidence points to additional pathological influences of activation of AT1R, in particular inflammation, fibrosis and atherosclerosis. The transcription factor nuclear factor κB, a key mediator in inflammation and atherosclerosis, can be activated by angiotensin II through a mechanism that may involve arrestin-dependent AT1 receptor internalization. Peritoneal dialysis is a therapeutic modality for treating patients with end-stage kidney disease. The effectiveness of peritoneal dialysis at removing waste from the circulation is compromised over time as a consequence of peritoneal dialysis-induced peritoneal fibrosis. The non-physiological dialysis solution used in peritoneal dialysis, i.e. highly concentrated, hyperosmotic glucose, acidic pH as well as large volumes infused into the peritoneal cavity, contributes to the development of fibrosis. Numerous trials have been conducted altering certain components of the peritoneal dialysis fluid in hopes of preventing or delaying the fibrotic response with limited success. We hypothesize that structural activation of AT1R by hyperosmotic peritoneal dialysis fluid activates the internalization process and subsequent signaling through the transcription factor nuclear factor κB, resulting in the generation of pro-fibrotic/pro-inflammatory mediators producing peritoneal fibrosis.

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Section: Peritoneal Dialysismentioning

confidence: 99%

Angiotensin II receptors and peritoneal dialysis-induced peritoneal fibrosis

Morinelli

Luttrell

Strungs

et al. 2016

The International Journal of Biochemistry & Cell Biology

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BmooMPα-I, a Metalloproteinase Isolated from Bothrops moojeni Venom, Reduces Blood Pressure, Reverses Left Ventricular Remodeling and Improves Cardiac Electrical Conduction in Rats with Renovascular Hypertension

Estrada

Rodrigues

Maciel

et al. 2022

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BmooMPα-I has kininogenase activity, cleaving kininogen releasing bradykinin and can hydrolyze angiotensin I at post-proline and aspartic acid positions, generating an inactive peptide. We evaluated the antihypertensive activity of BmooMPα-I in a model of two-kidney, one-clip (2K1C). Wistar rats were divided into groups: Sham, who underwent sham surgery, and 2K1C, who suffered stenosis of the right renal artery. In the second week of hypertension, we started treatment (Vehicle, BmooMPα-I and Losartan) for two weeks. We performed an electrocardiogram and blood and heart collection in the fourth week of hypertension. The 2K1C BmooMPα-I showed a reduction in blood pressure (systolic pressure: 131 ± 2 mmHg; diastolic pressure: 84 ± 2 mmHg versus 174 ± 3 mmHg; 97 ± 4 mmHg, 2K1C Vehicle, p < 0.05), improvement in electrocardiographic parameters (Heart Rate: 297 ± 4 bpm; QRS: 42 ± 0.1 ms; QT: 92 ± 1 ms versus 332 ± 6 bpm; 48 ± 0.2 ms; 122 ± 1 ms, 2K1C Vehicle, p < 0.05), without changing the hematological profile (platelets: 758 ± 67; leukocytes: 3980 ± 326 versus 758 ± 75; 4400 ± 800, 2K1C Vehicle, p > 0.05), with reversal of hypertrophy (left ventricular area: 12.1 ± 0.3; left ventricle wall thickness: 2.5 ± 0.2; septum wall thickness: 2.3 ± 0.06 versus 10.5 ± 0.3; 2.7 ± 0.2; 2.5 ± 0.04, 2K1C Vehicle, p < 0.05) and fibrosis (3.9 ± 0.2 versus 7.4 ± 0.7, 2K1C Vehicle, p < 0.05). We concluded that BmooMPα-I improved blood pressure levels and cardiac remodeling, having a cardioprotective effect.

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Evaluation of the use of captopril on peritoneal fibrosis induced in rats by the use of glucose solution 4.25%

Abstract: Our findings indicate that captopril do not decrease the intensity of fibrosis on the peritoneal membrane that happens on rats on peritoneal dialysis.

Cited by 2 publications

References 13 publications

Angiotensin II receptors and peritoneal dialysis-induced peritoneal fibrosis

Angiotensin II receptors and peritoneal dialysis-induced peritoneal fibrosis

BmooMPα-I, a Metalloproteinase Isolated from Bothrops moojeni Venom, Reduces Blood Pressure, Reverses Left Ventricular Remodeling and Improves Cardiac Electrical Conduction in Rats with Renovascular Hypertension

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