Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.23.15 (renin)
35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of extracorporeal shock waves on renal tissue, renal function, and blood pressure were studied by applying 500 shock waves to both kidneys in 72 female Wistar rats. Six groups, 12 rats in each, were sacrificed on days, 1, 7 and at months 1, 3, 6 and 12 after the procedure, when serum levels of BUN, creatinine, urine levels of beta 2-microglobulin (beta 2-MG), N-acetyl-beta-D-glucosaminidase (NAG), 28-kDa carbindin-D and creatinine clearance (Ccr) were determined. Findings were then compared with those from the control group. In each group, both kidneys were weighed and histologically evaluated. In the treatment group, systolic blood pressure was measured at post-irradiation months 1, 3, 6, 9, and 12; plasma renin activity was studied 6 and 12 months after irradiation to make evaluation in comparison with the control group. In the treatment group, histologically, coagulative necrosis associated with bleeding around the renal tubules and tubular epithelial cell degeneration were marked on day 1, but the glomerulus was kept in relatively good shape. Inflammatory cellular infiltration and interstitial fibrosis were noted on day 7 and the addition of scar formation 1 month after irradiation. Interstitial fibrosis, inflammatory cellular infiltration, scar formation, and tubular epithelial degeneration remained significant even after 12 months. In the treatment group, kidneys weighed significantly more than in the control group from day 1 through month 3, with edema likely accounting for this. However, weight then significantly declined 12 months after irradiation, owing to suspected scarring atrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of extracorporeal shock waves on renal morphology, renal function and blood pressure in rats--follow-up for one year]. 143 81

A double-blind crossover study versus placebo of the renal effects of the nonsteroidal anti-inflammatory drug imidazole 2-hydroxybenzoate was conducted in 10 patients with compensated liver cirrhosis. The administration of the drug (750 mg, t.i.d., for three days) did not affect renal plasma flow, glomerular filtration rate, free water clearance nor the urinary excretion of sodium or potassium. Values of plasma renin activity also did not change after drug administration. Direct tubular damage from imidazole 2-hydroxybenzoate was also excluded by normal excretion of beta-2-microglobulin and N-acetyl-beta-D-glucosaminidase. Urinary 6-keto-PGF1 alpha output were comparable during imidazole 2-hydroxybenzoate and placebo administration. These data indicate that this nonsteroidal antiinflammatory drug does not affect the renal function in patients with compensated liver cirrhosis.
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PMID:Renal effects of imidazole-2-hydroxybenzoate in patients with compensated liver cirrhosis. 150 25

To clarify the possible role of intrarenal renin-angiotensin system (RAS) in the evolution of renal hemodynamic alteration in diabetes, we investigated the change of tissue angiotensin-converting enzyme (ACE) activity, a key enzyme of RAS, in the kidneys obtained from streptozotocin-induced diabetic rats. Tissue ACE activity was significantly reduced in both outer cortex (0.29 +/- 0.04, mean +/- SEM, n = 6) and inner cortex with outer medulla (2.43 +/- 0.28, n = 6) of the kidneys from diabetic rats 2 weeks after induction of diabetes compared with those from control rats (0.47 +/- 0.05, n = 7, in outer cortex; 3.68 +/- 0.32, n = 7, in inner cortex with outer medulla). ACE activities in the lung and aorta of diabetic rats were not different from those of control rats. ACE activities in the serum and urine were significantly elevated in diabetic rats. Treatment of diabetic rats with insulin to achieve near euglycemia completely prevented these alterations in ACE activity, except that, in the urine, the elevation of ACE was partially corrected with insulin. In contrast to ACE activity, activity of N-acetyl-beta-D-glucosaminidase (a lysosomal enzyme of the tubule) and r-glutamyl transpeptidase (a brush border enzyme) in the kidney were not reduced in diabetic rats, whereas in the urine both enzyme activities were significantly elevated in diabetic rats. It is likely, therefore, that the reduction of ACE activity in the kidneys of diabetic rats may reflect the impairment of vascular endothelial cells in the kidney, rather than tubular damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduced activity of renal angiotensin-converting enzyme in streptozotocin-induced diabetic rats. 168 36

The renal effects of long-term antihypertensive treatment with enalapril were evaluated in 34 subjects (age, 53 yr; range, 27 to 65) with mild, uncomplicated hypertension. After receiving placebo for 4 wk, subjects were randomly assigned to groups receiving incremental doses of enalapril (10, 20, or 40 mg/day for 4 wk each) in a single morning dose or two divided doses, or of placebo. One subject who received enalapril developed acute renal failure by the end of the study. There was no evidence of glomerular or tubular damage in the other subjects; as measured by 24-hr urinary protein excretion, urinary activity of N-acetyl-beta-D-glucosaminidase, and uric acid clearance. During treatment with enalapril, renal plasma flow (measured with 131I-iodohippurate sodium) and glomerular filtration rate increased by 12.1% and 6.8%. Changes in renal plasma flow correlated inversely with age and final mean arterial pressure and correlated positively with initial plasma renin activity of subjects. Except for an occasional idiosyncratic adverse reaction, enalapril is a safe and effective antihypertensive drug with the unique ability to increase renal function despite a fall in renal perfusion pressure.
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PMID:Increased renal plasma flow in long-term enalapril treatment of hypertension. 631 77

The furosemide-induced increase in protein excretion, and its relations to 1) the size of protein molecules as reflected by three enzymes, and 2) glomerular filtration rate (GFR), plasma renin activity (PRA) and prostaglandin (PG) E2 and F2 alpha excretions were studied in 14 outpatients with normal renal function and 13 healthy males. Furosemide (120 mg) was given intravenously, and thereafter the protein excretion and the above parameters were monitored for 1--2 hours. In both groups, furosemide caused a transient increase in protein excretion. The excretion of the largest molecule, beta-glucuronidase, rose to 6.3-fold, while those of N-acetyl-beta-D-glucosaminidase and of the smallest molecule, alpha-amylase, increased by 91 and 37%, respectively. GFR increased, too, but markedly less than the protein excretion. PGE2 and PGF2 alpha excretions increased more than GFR and changed simultaneously with the excretion of proteins. Furosemide also caused a marked increase in PRA. This lasted, however, much longer than the rise in PG and protein excretion or GFR. The results suggest that the furosemide-induced increase in protein excretion is 1) related to the molecular size of proteins, 2) partly due to the rise in GFR, 3) simultaneous with the change in PG excretion. Our findings also agree with the view that furosemide causes changes in glomerular permeability.
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PMID:Increased urinary protein excretion after intravenous injection of furosemide in man. 700 92

We studied urine protein excretion in 55 adults with reflux nephropathy (median age 26.9 years) who had had normal blood pressure, renal function and ureteric reimplantation in childhood. Urine retinol binding protein (RBP), N-acetyl-beta-D-glucosaminidase (NAG), albumin, bacteriuria, systolic blood pressure, glomerular filtration rate (GFR), peripheral plasma renin activity (PRA) and the degree of renal scarring were measured in each subject; 20 had bilateral and 35 unilateral renal scarring; 5 were hypertensive and none were in renal failure. Urinary NAG and RBP excretions were significantly greater in the study group than in 34 healthy controls (median age 29.7 years). Within the study group, NAG excretion significantly correlated with PRA (P = 0.02). RBP excretion correlated with PRA, systolic blood pressure and the laterality (bilateral vs. unilateral) of scarring (P < 0.01). Urinary albumin excretion correlated with systolic blood pressure (P = 0.03). We conclude that increased urinary protein, especially NAG and RBP excretion, occur late after ureteric re-implantation in reflux nephropathy independent of GFR. Its association with PRA supports the concept of segmental perfusion and filtration as an important mechanism that may explain the above findings.
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PMID:Tubular proteinuria in reflux nephropathy: post ureteric re-implantation. 889 55

In rapidly growing male Sprague-Dawley rats with an initial body weight of 100 +/- 10 g, we investigated how alimentary magnesium (Mg) supply, Mg metabolism and ciclosporine (Ci)-associated nephrotoxicity are interrelated. Food with 100 ppm Mg (1Mg) or 1,000 ppm Mg (stMg) or 10,000 ppm Mg (rMg), Ci 20 mg/kg body weight daily or olive oil were applied for 3 months (n = 10/group). Mg concentrations in various compartments were measured by atomic absorption spectrophotometry. Creatinine clearance (Jaffe), urinary N-acetyl-beta-D-glucosaminidase (NAG) activity (fluorometrically), urinary sodium excretion (flame photometry) and osmolality were measured. Histomorphological examination was done and renal renin expression was studied by monoclonal antibodies. Ci reduced the Mg concentration of the femur under 1Mg (72.6 +/- 9.7 vs. 112.6 +/- 14.3 mmol/kg dry substance, p < 0.05) and under stMg (150.6 +/- 16.6 vs. 194.1 +/- 10.2 mmol/kg dry substance, p < 0.05), thus indicating Ci-related Mg deficiency. This was due to a significant increase in Mg excretion in Ci treatment compared to dietary controls. Under rMg, there was no difference between Ci-treated and control animals. Ci treatment lowered creatinine clearance in 1Mg (1.42 +/- 0.05 vs. 3.02 +/- 0.58 ml/min) and in stMg (1.04 +/- 0.45 vs. 2.18 +/- 0.51 ml/min), NAG/creatinine and urinary sodium excretion were negatively affected by Ci under 1Mg and stMg. Histomorphology showed macrocalcifications due to Mg deficiency and Ci-specific findings, which were markedly enhanced in 1Mg and stMg. Animals with plentiful Mg supply had no functional alterations due to Ci and no or weakly expressed histomorphological lesions. Renin-positive stained cells were higher in Ci-treated animals. This seems to be functionally relevant under 1Mg and stMg, since it was associated with sodium retention and elevated relative heart weight, indicating hypertension. Alimentary or drug-induced Mg deficiency plays a relevant role in the pathophysiology of chronic Ci nephrotoxicity. Our data suggest that Mg supplementation is helpful to reduce Ci toxicity, even if there is 'normal' alimentary Mg intake.
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PMID:Magnesium metabolism: basic aspects and implications of ciclosporine toxicity in rats. 890 62

The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is a new genetic model of non-insulin-dependent diabetes mellitus (NIDDM). We investigated whether treatment with an angiotensin II (ANGII) subtype-1 receptor antagonist delays the onset of NIDDM and attenuates diabetic nephropathy in the OLETF rat. OLETF rats fed a regular chow were treated with ANGII subtype-1 receptor antagonists (E4177 or TA606) for 22 weeks. Hemodynamic changes, glucose metabolism, and the effects on diabetic nephropathy were examined. Systolic blood pressure increased in OLETF rats in an age-dependent manner. OLETF rats exhibited increases in plasma concentrations of glucose and insulin and developed glucosuria at the age of 28 weeks. The changes in glucose metabolism were associated with proteinuria and an increase in urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG). Morphologic investigation revealed nodular lesions in glomeruli in the OLETF rats. The ANGII receptor antagonist treatment abolished the blood pressure elevation. However, the treatment did not affect plasma glucose and insulin levels and did not significantly reduce glucosuria. Nodular lesions in glomeruli were not improved by the treatment. However, the receptor antagonists significantly reduced proteinuria and urinary NAG excretion. Multivariate analyses revealed that proteinuria was determined by systolic blood pressure, lipid metabolism, and glucose levels in plasma. ANGII subtype-1 antagonism does not improve glucose metabolism in the OLETF rat model of NIDDM, which has abnormalities in the glucose-uptake system. Blood pressure elevation and part of the proteinuria associated with NIDDM depends on the renin-angiotensin system rather than glucose metabolisms per se.
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PMID:Angiotensin II subtype-1 receptor antagonists improve hemodynamic and renal changes without affecting glucose metabolisms in genetic rat model of non-insulin-dependent diabetes mellitus. 1007 80

Diabetic nephropathy is a leading cause of end-stage renal disease in industrialized countries. Although the molecular mechanisms for the development and progression of diabetic nephropathy are not fully understood, the formation of advanced glycation end products (AGEs) and activation of the renin-angiotensin system (RAS) have been considered to be the main factors participating in the pathogenesis of diabetic nephropathy. However, functional cross-talk between AGEs and the RAS remains to be elucidated. In this study, we examined the effects of oral administration of olmesartan medoxomil, a newly developed angiotensin II type 1 receptor antagonist, on renal damage in AGE-treated rats. Administration of olmesartan medoxomil significantly inhibited the increase of systolic and diastolic blood pressure levels and urinary N-acetyl-beta-D-glucosaminidase activity in exogenously AGE-injected rats. Furthermore, olmesartan medoxomil treatment also prevented glomerulosclerosis in AGE-treated rats. These results indicate that exogenous AGE treatment could induce renal damage via the activation of the RAS. Our study suggests that olmesartan medoxomil could be a valuable drug for the treatment of diabetic nephropathy by blocking the deleterious effects of AGEs.
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PMID:Olmesartan medoxomil, a newly developed angiotensin II type 1 receptor antagonist, protects against renal damage in advanced glycation end product (age)-injected rats. 1592 5

TG(mRen2)27 (Ren2) transgenic rats overexpress the mouse renin gene, with subsequent elevated tissue ANG II, hypertension, and nephropathy. The proximal tubule cell (PTC) is responsible for the reabsorption of 5-8 g of glomerular filtered albumin each day. Excess filtered albumin may contribute to PTC damage and tubulointerstitial disease. This investigation examined the role of ANG II-induced oxidative stress in PTC structural remodeling: whether such changes could be modified with in vivo treatment with ANG type 1 receptor (AT(1)R) blockade (valsartan) or SOD/catalase mimetic (tempol). Male Ren2 (6-7 wk old) and age-matched Sprague-Dawley rats were treated with valsartan (30 mg/kg), tempol (1 mmol/l), or placebo for 3 wk. Systolic blood pressure, albuminuria, N-acetyl-beta-D-glucosaminidase, and kidney tissue malondialdehyde (MDA) were measured, and x60,000 transmission electron microscopy images were used to assess PTC microvilli structure. There were significant differences in systolic blood pressure, albuminuria, lipid peroxidation (MDA and nitrotyrosine staining), and PTC structure in Ren2 vs. Sprague-Dawley rats (each P < 0.05). Increased mean diameter of PTC microvilli in the placebo-treated Ren2 rats (P < 0.05) correlated strongly with albuminuria (r(2) = 0.83) and moderately with MDA (r(2) = 0.49), and there was an increase in the ratio of abnormal forms of microvilli in placebo-treated Ren2 rats compared with Sprague-Dawley control rats (P < 0.05). AT(1)R blockade, but not tempol treatment, abrogated albuminuria and N-acetyl-beta-d-glucosaminidase; both therapies corrected abnormalities in oxidative stress and PTC microvilli remodeling. These data indicate that PTC structural damage in the Ren2 rat is related to the oxidative stress response to ANG II and/or albuminuria.
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PMID:Proximal tubule microvilli remodeling and albuminuria in the Ren2 transgenic rat. 1703 39


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