scholarly journals High-NaCl Diet Aggravates Cardiac Injury in Rats with Adenine-Induced Chronic Renal Failure and Increases Serum Troponin T Levels

2016 ◽  
Vol 6 (4) ◽  
pp. 317-327 ◽  
Author(s):  
Pavlos Kashioulis ◽  
Ola Hammarsten ◽  
Niels Marcussen ◽  
Emman Shubbar ◽  
Aso Saeed ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Cardiac Injury ◽  
Serum Levels ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Small Artery ◽  
Sprague Dawley Rats

Aims: To examine the effects of 2 weeks of high-NaCl diet on left ventricular (LV) morphology and serum levels of cardiac troponin T (cTnT) in rats with adenine-induced chronic renal failure (ACRF). Methods: Male Sprague-Dawley rats either received chow containing adenine or were pair-fed an identical diet without adenine [controls (C)]. Approximately 10 weeks after the beginning of the study, the rats were randomized to either remain on a normal NaCl diet (NNa; 0.6%) or to be switched to high-NaCl chow (HNa; 4%) for 2 weeks, after which acute experiments were performed. Results: Rats with ACRF showed statistically significant increases (p < 0.001) in arterial pressure (AP), LV weight and fibrosis, and serum cTnT levels compared to controls. Two weeks of high-NaCl intake augmented the increases in AP, LV weight and fibrosis, and serum cTnT concentrations only in ACRF rats (p < 0.05 for group × NaCl intake interaction). Compared to group C-NNa, cTnT levels were elevated approximately 6-fold in group ACRF-NNa and 24-fold in group ACRF-HNa. Focal LV injury with cardiomyocyte necrosis, scarring, and fibrinoid necrosis of small arteries were only detected in group ACRF-HNa. There was a strong correlation between the degree of LV fibrosis and serum cTnT levels in ACRF rats (r = 0.81, p < 0.01). Conclusion: Two weeks of high-NaCl diet in rats with ACRF produces LV injury and aggravates increases in serum cTnT levels, presumably by causing hypertension-induced small artery lesions leading to myocardial ischemia. This model may be suitable for studying pathophysiological mechanisms in chronic renicardiac syndromes.

Abstract 336: Rats with Adenine-Induced Chronic Renal Failure Develop Low-Renin Hypertension That is Aggravated by High NaCl Diet and Associated with Increased Aortic Stiffness

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Gregor Guron ◽  
Lisa Nguy ◽  
Maria Johansson ◽  
Tom Teerlink
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Aortic Stiffness ◽  
Control Diet ◽  
Plasma Renin ◽  
Aortic Pulse Wave Velocity ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Pronounced Increase ◽  
Low Renin Hypertension

We have shown that rats with adenine-induced chronic renal failure (A-CRF) develop modest hypertension, left ventricular hypertrophy, and a marked decrease in aortic relaxation rate. The aim of this study was to investigate mechanisms causing hypertension in this model and to assess aortic stiffness by measuring aortic pulse wave velocity (PWV). Male Sprague-Dawley rats were equipped with radiotelemetry probes and subsequently received either chow containing adenine (0.5% for 3 weeks, 0.3% for 2 w., and 0.15% thereafter) or were pair-fed with a normal control diet. At 7 to 11 weeks blood pressure responses to high NaCl diet (4%) and pharmacological interventions were performed. In separate groups aortic PWV was analyzed in isoflurane-anesthetized animals. Values are means±SD. Baseline 24-h mean arterial pressure (MAP) was 101±10 and 119±9 mmHg in controls and A-CRF animals, respectively (P < 0.01). After 5 days of 4% NaCl diet MAP had increased by 24±6 mmHg in A-CRF animals vs. 2±1 mmHg in controls (P<0.001 between groups). Administration of L-NAME in the drinking water (50 mg/kg/day) increased MAP by 37±9 and 24±4 mmHg in A-CRF animals and controls, respectively (P< 0.01 between groups). Candesartan (10 mg/kg by gavage) produced a more pronounced reduction of MAP in controls vs. A-CRF animals (-12±3 vs. -5±5 mmHg, P<0.05). Aortic PWV was elevated in A-CRF rats (5.10±0.51 vs. 4.58±0.17 m/s, P<0.05) although histological analysis did not show aortic calcifications. At sacrifice, plasma levels of creatinine (259±46 vs. 31±2 μM, P<0.001) and asymmetric dimethylarginine (ADMA, 0.65±0.04 vs. 0.45±0.02 μM, P < 0.001) were elevated in A-CRF animals whereas plasma renin activity was markedly suppressed (0.7±0.5 vs. 15.1±7.5 μg/L/h, P<0.001). Hypertension in A-CRF animals is characterized by low renin levels and is aggravated by high NaCl diet suggesting a pathogenic role for hypervolemia secondary to severe renal insufficiency. Although ADMA concentrations were elevated, A-CRF animals showed a more pronounced increase in MAP in response to L-NAME than controls, suggesting that reduced nitric oxide synthase activity was not a major cause of hypertension in this model. Finally, aortic stiffness was elevated in A-CRF animals as indicated by increased aortic PWV.

scholarly journals iTRAQ-Based Proteomics of Chronic Renal Failure Rats after FuShengong Decoction Treatment Reveals Haptoglobin and Alpha-1-Antitrypsin as Potential Biomarkers

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Yu Yang ◽  
Junmeng Wei ◽  
Xuekuan Huang ◽  
Mingjun Wu ◽  
Zhenbing Lv ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Differentially Expressed ◽  
Coagulation Cascade ◽  
Control Group ◽  
Differentially Expressed Proteins ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Alpha 1 Antitrypsin ◽  
Global Health Problem

Background. Chronic renal failure (CRF) has become a global health problem and bears a huge economic burden. FuShengong Decoction (FSGD) as traditional Chinese medicine has multiple pharmacological effects. Objectives. To understand the underlying molecular mechanism and signaling pathway involved in the FSGD treatment of CRF and screen differentially expressed proteins in rats with CRF treated with FSGD. Methods. Thirty-three male Sprague-Dawley rats were randomly divided into control group, CRF group, and FSGD group. Differentially expressed proteins were screened by iTRAQ coupled with nanoLC-MS/MS, and these identified proteins were later analyzed by GO, KEGG, and STRING. Additionally, haptoglobin (HP) and alpha-1-antitrypsin (AAT) were finally verified by ELISA, Western blot, and real time PCR. Results. A total of 417 proteins were identified. Nineteen differentially expressed proteins were identified in the FSGD group compared with the model group, of which 3 proteins were upregulated and 16 proteins were downregulated. Cluster analysis indicated that inflammatory response was associated with these proteins and complement and coagulation cascade pathways were predominantly involved. The validation methods further confirmed that the levels of HP and AAT were significantly increased. Conclusions. HP and AAT may be the important biomarkers in the pathogenesis of CRF and FSGD therapy.

scholarly journals Curcumin prevents cardiac remodeling secondary to chronic renal failure through deactivation of hypertrophic signaling in rats

2010 ◽  
Vol 299 (4) ◽  
pp. H975-H984 ◽  
Author(s):  
Siddhartha S. Ghosh ◽  
Fadi N. Salloum ◽  
Antonio Abbate ◽  
Richard Krieg ◽  
Domenic A. Sica ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Signaling Pathways ◽  
Glycogen Synthase ◽  
Vena Cava ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Activated T Cells ◽  
Hypertrophic Response ◽  
Hypertrophic Signaling

The prevalence of left ventricular hypertrophy (LVH) is frequent in patients with end-stage renal disease following chronic renal failure (CRF). We investigated the therapeutic efficacy of curcumin, the principal curcuminoid of the Indian curry spice turmeric, in attenuation of LVH and sought to delineate the associated signaling pathways in blunting the hypertrophic response in nephrectomized rats. Adult Sprague-Dawley rats underwent nephrectomy (Nx) by removal of 5/6 of the kidneys. Four groups were studied for 7 wk: 1) control (sham), 2) Nx, 3) Nx + curcumin (150 mg/kg bid), and 4) Nx + enalapril (15 mg/kg bid) as positive control. Subtotal nephrectomy caused renal dysfunction, as evidenced by a gradual increase in proteinuria and elevation in blood urea nitrogen and plasma creatinine. Nx rats showed a significant hypertrophic response and increased diameter of inferior vena cava at inspiration, which was inhibited by treatment with curcumin or enalapril. Moreover, the Nx rats demonstrated changes in the signaling molecules critically involved in the hypertrophic response. These include increased glycogen synthase kinase-3β phosphorylation, β-catenin expression, calcineurin, phosphorylated (p) nuclear factor of activated T cells, pERK, and p-cAMP-dependent kinase. Both curcumin and enalapril variably but effectively deactivated these pathways. Curcumin attenuates cardiac hypertrophy and remodeling in nephrectomized rats through deactivation of multiple hypertrophic signaling pathways. Considering the safety of curcumin, these studies should facilitate future clinical trials in suppressing hypertrophy in patients with CRF.

Amelioration with vessel dilator of acute tubular necrosis and renal failure established for 2 days

2000 ◽  
Vol 278 (5) ◽  
pp. H1555-H1564 ◽  
Author(s):  
Linda C. Clark ◽  
Hanan Farghaly ◽  
Sabiha R. Saba ◽  
David L. Vesely
Keyword(s):  
Renal Failure ◽  
Acute Tubular Necrosis ◽  
Peptide Hormone ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Ventricular Dilation ◽  
Water Excretion ◽  
Tubular Necrosis ◽  
Sprague Dawley Rats ◽  
Left Ventricular Dilation

Seventeen Sprague-Dawley rats had ischemic nonoliguric acute renal failure (ARF) induced by vascular clamping resulting in their preischemic blood urea nitrogen (BUN) and creatinine levels of 16 ± 1 and 0.56 ± 0.05 mg/dl to increase to 162 ± 4 and 8.17 ± 0.5 mg/dl, P < 0.001, respectively, at day 4 of postischemia. Vessel dilator, a 37-amino-acid cardiac peptide hormone (0.3 μg ⋅ kg− 1 ⋅ min− 1ip), decreased the BUN and creatinine levels to 53 ± 17 mg/dl and 0.98 ± 0.12 mg/dl ( P < 0.001) in another seven animals where ARF had been established for 2 days. Water excretion doubled with ARF and was further augmented by vessel dilator. Transthoracic echocardiography revealed left ventricular dilation as a probable cause of the increase in vessel dilator in the circulation with ARF, and vessel dilator infusion reversed this dilation. At day 6 of ARF, mortality decreased to 14% with vessel dilator from 88% without vessel dilator. Acute tubular necrosis was <5% in the vessel dilator-treated rats compared with 25% to >75% in the placebo-treated ARF animals. We conclude that vessel dilator improves acute tubular necrosis and renal function in established ARF.

scholarly journals Altered norepinephrine turnover in the brain of rats with chronic renal failure.

1994 ◽  
Vol 4 (11) ◽  
pp. 1901-1907
Author(s):  
R Bigazzi ◽  
E Kogosov ◽  
V M Campese
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Locus Coeruleus ◽  
Turnover Rate ◽  
Nucleus Tractus Solitarius ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Norepinephrine Turnover ◽  
Hypothalamic Nuclei ◽  
And Control

Disturbances of the sympathetic nervous system have been described in chronic renal failure, but their role in the genesis and maintenance of hypertension frequently associated with this condition has not been established. The neuroadrenergic activity in brain nuclei involved in the regulation of blood pressure in uremic animals has also not been previously evaluated. In these studies, the neuroadrenergic activity was measured in the anterior, lateral, and posterior hypothalamic nuclei, in the locus coeruleus, and in the nucleus tractus solitarius of Sprague Dawley rats 5/6 nephrectomized or sham operated 4 wk before the experiments. Neuroadrenergic activity was determined by calculating norepinephrine (NE) turnover rate (in picograms per milligram per hour), 3, 6 and 12 h after inhibition of NE synthesis with L-methyltyrosine. The endogenous NE concentration was significantly greater in the posterior hypothalamic nuclei (21,501 +/- 1,777 pg/mg wet wt) and in the locus coeruleus (16,152 +/- 1,114 pg/mg wet tissue) of uremic compared with control rats (12,213 +/- 1,404 and 7,991 +/- 622 pg/mg wet wt, respectively). On the other hand, the endogenous NE content of the nucleus tractus solitarius and the anterior hypothalamic nuclei did not differ between uremic and control rats. The turnover rate of NE in the posterior hypothalamic nuclei of uremic rats (2150 +/- 430 pg/mg per hour) was significantly faster (P < 0.05) than in control rats (977 +/- 244 pg/mg per hour). The turnover rate of NE in the locus coeruleus of uremic rats (2,584 +/- 323 pg/mg per hour) was also significantly faster than in control animals (400 +/- 140 pg/mg per hour; P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Doxorubicin-Induced Cardiac Abnormalities in Rats: Attenuation via Sandalwood Oil

Pharmacology ◽  
2019 ◽  
Vol 105 (9-10) ◽  
pp. 522-530 ◽  
Author(s):  
Nancy S. Younis
Keyword(s):  
Inflammatory Response ◽  
Troponin T ◽  
Cardiac Injury ◽  
Cardiac Biomarkers ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Group 4 ◽  
Sprague Dawley Rats ◽  
Sandalwood Oil ◽  
Group 2

<b><i>Introduction:</i></b> The clinical use of doxorubicin (DOX) is challenged by its incremental dose-related cardiotoxicity. <b><i>Objective:</i></b> The aim of the hereby study was to investigate sandalwood essential oil (SEO) against DOX-induced cardiac toxicity. <b><i>Methods:</i></b> Male Sprague-Dawley rats were allocated into 4 groups. Groups 1 signified the control, whereas group 2 administered 100 mg/kg/day SEO, both act as control. In group 3, DOX was given intraperitoneal in a dose of 3 mg/kg/ every other day for 2 weeks to induced cardiotoxicity. While group 4 received a combination of SEO and DOX for 2 weeks. DOX prompted variations were assessed by measuring cardiac injury biomarkers, including creatine phosphokinase, cardiac troponin T, and lactate dehydrogenase (LDH), electrocardiogram (ECG) fluctuations, heart rate (HR), and blood pressure (BP) indices. The effect of both DOX and SEO on various antioxidants such as glutathione, superoxide dismutase, and catalase and inflammatory mediators including interleukin-1β, tumor necrosis factor-alpha, and NF-κB was quantified. <b><i>Results:</i></b> DOX augmented cardiac injury biomarkers, altered ECG, deceased HR and antioxidants, and finally increased BP indices. Treatment with SEO significantly (<i>p</i> &#x3c; 0.05) decreased cardiac biomarkers and reversing ECG changes and BP. Moreover, treatment with SEO enhanced HR anomalies and antioxidant activity reduction and precluded the intensive inflammatory response induced by DOX. <b><i>Conclusion:</i></b> SEO may have the potential of mitigating cardiac rhythm and BP indices changes induced with DOX. SEO modifications may be due to antioxidant capacity improvement and inflammatory response prohibition of the heart muscle.

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