Biochemical changes in the pancreas of rats with chronic renal failure

1985 ◽  
Vol 249 (4) ◽  
pp. F518-F523
Author(s):  
G. A. Kaysen ◽  
A. P. Majumdar ◽  
M. A. Dubick ◽  
G. D. Vesenka ◽  
G. Mar ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
The Other ◽  
Sprague Dawley ◽  
Pancreatic Acini ◽  
Cholecystokinin Octapeptide ◽  
Dna And Rna ◽  
Sprague Dawley Rats ◽  
Cationic Trypsinogen ◽  
Protease Inhibitory Activity

Chronic renal failure (CRF) was produced in female Sprague-Dawley rats by 7/8 nephrectomy. Creatinine clearance was depressed significantly (P less than 0.005) and blood urea nitrogen (BUN) increased in CRF rats when compared with the sham-operated (S) controls. CRF caused no apparent change in body weight but significantly increased pancreatic weight as well as increased DNA, RNA, and protein content. Pancreatic protein-to-DNA and RNA-to-DNA ratios were also found to be significantly higher in CRF rats than in the S controls. Trypsin-like activity and immunoreactive cationic trypsinogen levels were both increased in the pancreas of CRF rats, but not in their serum. On the other hand, protease inhibitory activity in the pancreas and serum was significantly decreased by CRF. The ability of the dispersed pancreatic acini isolated from CRF rats to incorporate [3H]-leucine into protein, in the absence and presence of 0.25 nM cholecystokinin octapeptide (CCK-8), was found to be lower than in the controls. Furthermore, discharge of both trypsinogen and chymotrypsinogen induced by CCK-8 was markedly reduced from acini of CRF rats as compared with the S controls. In contrast, lactate dehydrogenase (LDH) was released more readily from pancreatic acini of CRF. It is concluded that mild CRF produces hyperplasia and hypertrophy of the pancreas and lowers the responsiveness of acini to CCK-8 with respect to synthesis and secretion of proteins.

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 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)

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 Familial Atypical Hemolytic Uremic Syndrome with Positive pS1191L (c.3572C> T) Mutation in CFH A Single-Center Experience

2019 ◽  
Author(s):  
Fadime ERSOY DURSUN ◽  
Gözde YESIL ◽  
Hasan DURSUN ◽  
Gülşah SASAK
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Family History ◽  
Hemolytic Uremic Syndrome ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Gene Mutations ◽  
Factor H ◽  
The Other ◽  
History Of ◽  
Uremic Syndrome

Abstract Background: Atypical hemolytic uremic syndrome is a condition characterized by thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury, which can exhibit a poor prognosis. Gene mutations play a key role in this disease, which may be sporadic or familial. Methods: We studied, 13 people from the same family were investigated retrospectively for gene mutations of familial atypical hemolytic uremic syndrome after a patient presented to our emergency clinic with atypical hemolytic uremic syndrome and reported a family history of chronic renal failure. Results: The pS1191L mutation in the complement factor H gene was heterozygous in 6 people from the family of the patient with atypical hemolytic uremic syndrome. One of these people was our patient with acute renal failure and the other two are followed up by the Nephrology Clinic due to chronic renal failure. The other 3 persons showed no evidence of renal failure. The index case had a history of 6 sibling deaths; two of them died of chronic renal failure. Plasmapheresis and fresh frozen plasma treatment was given to our patient. When patient showed no response to this treatment, eculizumab therapy was started. Conclusions: The study demonstrated that a thorough family history should be taken in patients with atypical hemolytic uremic syndrome. These patients may have familial type of the disease and they should be screened genetically. Eculizumab should be the first choice in the treatment with plasmapheresis. It should be kept in mind that the use of eculizumab as prophylaxis in post-transplant therapy is extremely important for prevention of rejection.

Cholecystokinin satiety involves CCKA receptors perfused by the superior pancreaticoduodenal artery

1998 ◽  
Vol 274 (5) ◽  
pp. R1390-R1396 ◽  
Author(s):  
James E. Cox
Keyword(s):  
Receptor Antagonist ◽  
Food Deprivation ◽  
Jugular Vein ◽  
Sucrose Intake ◽  
Sprague Dawley ◽  
Pancreaticoduodenal Artery ◽  
Cholecystokinin Octapeptide ◽  
Sprague Dawley Rats ◽  
Within Subjects ◽  
Ccka Receptors

Three experiments compared the potency of the type A cholecystokinin (CCKA)-receptor antagonist devazepide for increasing intake of 30% sucrose when injected into the superior pancreaticoduodenal (SPD) artery (SPD group) or jugular vein (IV group). In experiment 1, 15 min of sucrose intake in adult, male Sprague-Dawley rats after 6 h of food deprivation was increased by devazepide (20 μg/kg) administered into the SPD artery whether given alone or in conjunction with cholecystokinin octapeptide (CCK-8, 2 μg/kg ip). Devazepide had no effect in the IV group. In experiment 2, injection of 8, 20, and 50 μg/kg of devazepide into the SPD artery increased sucrose intake of nondeprived rats. Only the highest dose was effective in the IV group. On subsequent tests, administration of 1 μg/kg of CCK-8 significantly suppressed intake only in the SPD group. In experiment 3, nondeprived rats with SPD artery and jugular vein catheters were tested in a within-subjects design. Devazepide (20 μg/kg) increased sucrose intake after injection into the SPD artery, but not into the jugular vein. In experiment 4, intraduodenal devazepide (8, 20, and 50 μg/kg) had no effect. These results indicate that CCKA receptors within the SPD arterial bed mediate the satiating action of CCK, consistent with local action of duodenal CCK.

Regional effect of naltrexone in the nucleus of the solitary tract in blockade of NPY-induced feeding

2000 ◽  
Vol 278 (2) ◽  
pp. R499-R503 ◽  
Author(s):  
C. M. Kotz ◽  
M. J. Glass ◽  
A. S. Levine ◽  
C. J. Billington
Keyword(s):  
Cerebrospinal Fluid ◽  
Food Intake ◽  
Paraventricular Nucleus ◽  
Opioid Receptors ◽  
The Other ◽  
Solitary Tract ◽  
Sprague Dawley ◽  
Regional Effect ◽  
Sprague Dawley Rats ◽  
Artificial Cerebrospinal Fluid

Naltrexone (NLTX) in the nucleus of the solitary tract (NTS) decreases feeding induced by neuropeptide Y (NPY) in the paraventricular nucleus (PVN). We sought to determine the NTS region most sensitive to NLTX blockade of PVN NPY-induced feeding. Male Sprague-Dawley rats were fitted with two cannulas; one in the PVN and one in a hindbrain region: caudal, medial, or rostral NTS or 1 mm outside the NTS. Animals received NLTX (0, 1, 3, 10, and 30 μg in 0.3 μl) into the hindbrain region just prior to PVN NPY (0.5 μg, 0.3 μl) or artificial cerebrospinal fluid (0.3 μl). Food intake was measured at 2 h following injection. PVN NPY stimulated feeding, and NLTX in the medial NTS significantly decreased NPY-induced feeding at 2 h, whereas administration of NLTX in the other hindbrain regions did not significantly influence PVN NPY induced feeding. These data suggest that opioid receptors in the medial NTS are most responsive to feeding signals originating in the PVN after NPY stimulation.

scholarly journals Protein-to-creatinine urinary in the early diagnosis of renal injury in canine pyometra

2019 ◽  
Vol 39 (3) ◽  
pp. 186-191
Author(s):  
Marcos C. Sant’Anna ◽  
Guilherme F. Martins ◽  
Karina K.M.C. Flaiban ◽  
Luiz G.C. Trautwein ◽  
Maria I.M. Martins
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Injury ◽  
Renal Damage ◽  
Systemic Disease ◽  
The Other ◽  
Control Group ◽  
Creatinine Ratio ◽  
Renal Lesions ◽  
Tubular Cells

ABSTRACT: Kidney disease that affects bitches with pyometra may lead patients to develop chronic renal failure even after pyometra treatment. Therefore, several studies have sought to clarify the gaps in the understanding of the pathogenesis of renal injury in pyometra. Identification of early detection markers for renal damage, which can predict and identify the prognosis of the disease, is very important. Proteinuria analysis can diagnose kidney damage, since proteins such as albumin are not filtered through the glomerulus and those that undergo glomerular filtration are almost completely reabsorbed by tubular cells. The objective of this study was to evaluate whether the urinary protein-to-creatinine ratio (UPC) can detect renal injury in bitches with pyometra before development of azotemia. For this, 44 bitches with pyometra were divided into two groups: bitches with azotemic piometra (A, n=15, creatinine >1.7) and bitches with non-azotemic pyometra (NA, n=29). The two groups were compared to the control group (CG, n=12), which had no signs of systemic disease. All animals underwent blood and urine tests. Leukocytosis was more evident in bitches in the A group than in the other groups. This shows that the inflammatory response may be associated with the pathogenesis of renal injury. The median UPC in bitches with pyometra was significantly higher than in the CG, with a median above the reference values. In conclusion, the UPC can be used in bitches with pyometra to detect renal damage before the development of azotemia. It has been suggested that the UPC of bitches with pyometra should be followed through during the postoperative period so that permanent renal lesions secondary to pyometra can be diagnosed and treated properly before the development of azotemia.

Endogenous vasopressin regulates Na-K-ATPase and Na+-K+-Cl− cotransporterrbsc-1 in rat outer medulla

2002 ◽  
Vol 282 (2) ◽  
pp. F265-F270 ◽  
Author(s):  
Claudia A. Bertuccio ◽  
Fernando R. Ibarra ◽  
Jorge E. Toledo ◽  
Elvira E. Arrizurieta ◽  
Rodolfo S. Martin
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Atpase Activity ◽  
Receptor Antagonist ◽  
The Other ◽  
Outer Medulla ◽  
Physiological Conditions ◽  
Increased Activity ◽  
Expression And Activity

Previous reports have shown a stimulatory effect of vasopressin (VP) on Na-K-ATPase and rBSC-1 expression and activity. Whether these VP-dependent mechanisms are operating in vivo in physiological conditions as well as in chronic renal failure (CRF) has been less well studied. We measured ATPase expression and activity and rBSC-1 expression in the outer medulla of controls and moderate CRF rats both before and under in vivo inhibition of VP by OPC-31260, a selective V2-receptor antagonist. OPC-31260 decreased Na-K-ATPase activity from 11.2 ± 1.5 to 3.7 ± 0.8 in controls ( P < 0.05) and from 19.0 ± 0.8 to 2.9 ± 0.5 μmol Pi · mg protein−1 · h−1 in moderate CRF rats ( P < 0.05). CRF was associated with a significant increase in Na-K-ATPase activity ( P < 0.05). Similarly, CRF was also associated with a significant increase in Na-K-ATPase expression to 164.4 ± 21.5% compared with controls ( P < 0.05), and OPC-31260 decreased Na-K-ATPase expression in both controls and CRF rats to 57.6 ± 9.5 and 105.3 ± 10.9%, respectively ( P < 0.05). On the other hand, OPC-31260 decreased rBSC-I expression in both controls and CRF rats to 60.8 ± 6.5 and 30.0 ± 6.9%, respectively ( P < 0.05), and was not influenced by CRF (95.7 ± 5.2%). We conclude that 1) endogenous VP modulated Na-K-ATPase and rBSC-1 in both controls and CRF; and 2) CRF was associated with increased activity and expression of the Na-K-ATPase in the outer medulla, in contrast to the unaltered expression of the rBSC-1. The data suggest that endogenous VP could participate in the regulation of electrolyte transport at the level of the outer medulla.

EXCRETION OF CATECHOL AMINES BY WHITE RATS IN THE COLD

1964 ◽  
Vol 42 (4) ◽  
pp. 567-577 ◽  
Author(s):  
Lorraine C. Smith ◽  
L.-P. Dugal
Keyword(s):  
The Other ◽  
Sprague Dawley ◽  
White Rats ◽  
Sprague Dawley Rats ◽  
Old Rats ◽  
Catechol Amines ◽  
Sustained Increase

Exposure of white rats to 2 °C for 20 weeks caused an immediate and sustained increase in the excretion of catechol amines as compared to controls kept at 23 °C. Adrenaline excretion increased approximately three to four times while noradrenaline excretion increased about eight times. There were no marked differences between Wistar and Sprague–Dawley rats in the amounts of adrenaline and noradrenaline excreted at 23 °C or 2 °C. 'Old' rats kept in activity cages excreted much more of the catechol amines both at 23 °C and 2 °C than did the other rats and they showed a peak for adrenaline excretion after 1 week and for noradrenaline excretion after 3 to 4 weeks in the cold.

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