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:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urea-denatured alpha-zein was almost completely hydrolyzed into small peptides by digestion with 1/100 (w/w) of thermolysin at 37 degrees C for 3h. The angiotensin I-converting enzyme (ACE) inhibitory activity (IC50) of the thermolysin digest of total alpha-zein was 24.5 micrograms/ml, and most of the peptide fractions from Z19 alpha-zein and total alpha-zein separated by reverse-phase HPLC had more or less ACE inhibitory activity. From these fractions, thirty-six peptides, including 5 dipeptides, 14 tripeptides, 9 tetrapeptides, 5 pentapeptides, and 3 hexapeptides, were purified and their amino acid sequences were determined.
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PMID:Isolation from alpha-zein of thermolysin peptides with angiotensin I-converting enzyme inhibitory activity. 882 36

Benazepril (BP), an angiotensin convertive enzyme inhibitor, was administered orally once daily for 4 weeks to 31 dogs with mild to moderate (NYHA functional classes II and III) congestive heart failure caused from mitral insufficiency (MI). There were no significant changes in clinical signs, electrocardiogram findings, radiographical observations and plasma biochemical results in 11 dogs treated with placebo for 4 weeks. In 31 dogs treated with BP, appetite increased, and mean scores of heart failure signs, such as activity, exercise tolerance, cough and respiratory effort, were significantly improved. No dog displays signs suggesting systemic hypotension. One dog died suddenly on the 26th day of treatment with BP. This dog had good vigor and appetite till the evening before the death, and cough and exercise tolerance had been gradually improving. The heart rate and ECG parameters of BP treated dogs did not change significantly, but length of long axis of the heart decreased. In plasma biochemical tests, plasma urea nitrogen (UN) levels did not change significantly, and plasma creatinine (CRE) levels increased slightly within the normal ranges during BP trial. Two dogs had higher plasma UN levels with slightly higher plasma CRE levels, but had normal general condition and other biochemical results. Plasma ACE activity decreased to 57.3% of pre-treatment level at 4 weeks after BP treatment. It is concluded that BP monotherapy was efficacious at least in dogs with relatively low grade congestive heart failure caused by MI.
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PMID:Efficacy of monotherapy with benazepril, an angiotensin converting enzyme inhibitor, in dogs with naturally acquired chronic mitral insufficiency. 927 44

The effect of blockade of the renin-angiotensin system on kidney function using non-peptide angiotensin AT1 receptor antagonists was investigated in renovascular hypertensive rats. An angiotensin converting enzyme inhibitor, captopril and two angiotensin AT1 receptor antagonists, losartan and GR138950 (1-([3-bromo-2[2-[[(trifluoro-methyl)sulphonyl]amino]phenyl]-5 benzofuranyl]methyl)-4-cyclopropyl-2-ethyl-1H-imidazole-5-carboxamide) were administered in Na+-deplete two-kidney, two-clip Goldblatt hypertensive rats over a 3-day period. Captopril, losartan (30 mg/kg body weight) and GR138950 (5 mg/kg body weight) significantly (P < 0.001) lowered the systolic blood pressure in the hypertensive rats from 290 +/- 5, 252 +/- 9 and 238 +/- 13 mmHg to 152 +/- 17, 148 +/- 9 and 123 +/- 6 mmHg, respectively. The magnitude of reduction in blood pressure in these three groups of rats was similar and occurred with comparable marked increases in plasma levels of urea and creatinine indicative of acute renal failure. These findings demonstrate an important role for angiotensin II in the maintenance of renal function during blood pressure reduction in renovascular hypertensive states during restriction of dietary Na+ intake.
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PMID:The effect of angiotensin II receptor antagonists on kidney function in two-kidney, two-clip Goldblatt hypertensive rats. 927 78

Cardiovascular diseases are the most common causes of mortality, and hypertension is the most common cardiovascular disease in all ages. The Systolic Hypertension in the Elderly Program (SHEP) trial has shown that the pharmacologic reduction of isolated systolic hypertension can significantly reduce the incidence of cardiovascular complications. The aim of the Italian multicenter study reported here is to compare the efficacy, safety, and tolerability of fosinopril, a novel angiotensin converting enzyme (ACE) inhibitor with a dual route of excretion, with chlorthalidone, the diuretic administered in the SHEP study, in 312 elderly patients with isolated systolic hypertension. Our results show that fosinopril and chlorthalidone produce identical and statistically significant reductions in systolic blood pressure (-23.9 +/- 11.6 mm Hg and -23.7 +/- 10.9 mm Hg, respectively) and, to a lesser extent, in diastolic blood pressure (-7.1 +/- 3.1 mm Hg and -5.2 +/- 2.3 mm Hg, respectively). Only chlorthalidone caused a statistically significant change in uric acid, total cholesterol, blood urea, and serum potassium concentrations. Fosinopril was also somewhat better tolerated than chlorthalidone. In conclusion, the novel ACE inhibitor fosinopril is an effective and well-tolerated antihypertensive agent for use in elderly patients with isolated systolic hypertension and appears to be a suitable alternative for the treatment of isolated systolic hypertension.
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PMID:An effective approach for treating elderly patients with isolated systolic hypertension: results of an Italian multicenter study with fosinopril. 936 78

Author investigated the safety of combined ACE inhibitor (captopril) and spironolacton therapy on 237 pts with severe heart failure (NYHA III-IV.) treated with digitalis and loop diuretic during on average 65.4 months follow-up period. Incidence of clinically significant increase in serum urea, creatinine and potassium level was evaluated and compared with those of in group treated 47 pts with the same standard therapy captopril, digitalis, furosemide, without spironolacton. There was no significant difference between the incidence of azotemia and hyperkalemia in the two groups. The author emphasizes on the base of their results the safety of combined captopril and low dose spironolactone therapy in heart failure.
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PMID:[Effect of combined captopril-spironolactone therapy of cardiac insufficiency on kidney function and serum electrolyte values]. 945 4

The present study was designed to investigate the effect of captopril, a sulfhydryl (-SH) containing ACE inhibitor and lisinopril, a non-SH containing ACE inhibitor, on ischaemia-reperfusion-induced renal injury in rats and to study the involvement of the free radical scavenging property of captopril in its renoprotective effect. Bilateral renal artery occlusion was induced for 30 min followed by reperfusion for 24 h. Blood samples were taken from retro orbital sinus before surgery and at 24 h after reperfusion for blood urea and blood creatinine estimation. After completion of 24 h of renal reperfusion the carotid artery was cannulated and the mean arterial blood pressure (MABP) was recorded. The left kidney was used for histological examination. The right kidney was utilised for estimation of mitochondrial thiobarbituric acid reactive substances (TBARS). Renal ischaemia, followed by reperfusion, significantly increased blood urea nitrogen (BUN) and blood creatinine. However, creatinine clearance decreased markedly. Captopril administered before renal artery occlusion or immediately after reperfusion and lisinopril pre-treatment significantly attenuated the increase in BUN and blood creatinine. Creatinine clearance was markedly better in captopril-treated animals as compared to lisinopril-treated rats. Captopril significantly decreased the degree of tubular necrosis, haemorrhagic streaks and urinary casts. Lisinopril treatment decreased tubular necrosis and urinary casts but no marked effect on haemorrhagic streaks was noted. Administration of captopril before ischaemia or just after reperfusion significantly reduced the elevated concentration of mitochondrial TBARS but no such decrease was noted in lisinopril-treated rats. Based on these results it may be concluded that captopril and lisinopril markedly protected against ischaemia-reperfusion-induced renal injury and any additional renoprotective effect of captopril may be ascribed to its free radical scavenging properties.
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PMID:Effect of angiotensin converting enzyme inhibitors on ischaemia-reperfusion-induced renal injury in rats. 950 76

The CASSIS study was a double-blind multicentric controlled Czech and Slovak study focused on treatment of chronic heart failure with the ACE inhibitor spirapril; it was conducted for 12 weeks. The present work analyzes the second year of the extended open part of the study when all patients (n = 168) were treated with 3 mg or 6 mg spirapril. A small proportion of the patients was treated with 12 mg spirapril. The objective of the study was to test the long-term effectiveness and tolerance of spirapril. The general mortality was analyzed throughout the whole two-year period. The results revealed an unchanging total mortality, analyzed after three-month intervals, during the whole two-year period. Also the functional improvement of the patients according to NYHA which occurred after the first three months of treatment was preserved during the second year. Spirapril proved to be a well tolerated ACE-inhibitor. The authors did not observe angioneurotic oedema in any of the patients. Hypotension and cough were recorded in 0.6% of the patients. The incidence of undesirable laboratory effects was also low and the majority was due to the basic disease. Creatinine did not rise significantly and a rise of urea was observed only in a small number of patients. Liver functions and haemogram did not change during treatment. The results of the second year of erxtension indicate that spirapril is a very effective and safe ACE-inhibitor which will extend in a significant way therapeutic means in patients with chronic heart failure.
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PMID:[Therapy of heart failure with spirapril--the open phase of the CASSIS study. Analysis of the 2nd year extension of the CASSIS study]. 960 64

The nephrotic mouse (ICGN strain) is a useful model for progressive nephrotic syndrome (NS). In the present study, we demonstrated the preventive effects of enalapril, an angiotensin converting enzyme (ACE) inhibitor, on the progression of renal dysfunction and tubulo-interstitial fibrosis in the NS mice. Administration of enalapril (5 mg/dL in drinking water) to the 4-week-old NS mice for a 4-week-period did not improve their nephrotic symptoms such as albuminuria and hypoalbuminemia, but significantly suppressed the increases in blood urea nitrogen and serum creatinine levels. Renal histopathology demonstrated that the administration of the ACE inhibitor significantly attenuated the progression of the tubular and interstitial lesions (tubular dilatation, luminal cast accumulation and interstitial expansion) rather than the glomerular sclerotic changes. The suppression of the increase in blood urea nitrogen level by enalapril depended on the attenuated tubular injury rather than on the unchanged glomerular matrix deposition. Immunohistochemical examination revealed that the administration of the ACE inhibitor suppressed the formation of myofibroblasts, identified by the alpha-smooth muscle actin-positive cells, in the interstitial spaces. Consequently, interstitial matrix deposition was significantly reduced in the NS mice treated with enalapril. From the results obtained with the spontaneous nephrotic model, we emphasize a possibility that ACE inhibitor may be effective for attenuating progression of renal dysfunction and fibrosis in human NS, even if the ACE inhibitor fails to improve nephrotic symptoms such as albuminuria and hypoalbuminemia.
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PMID:Preventive effect of ACE inhibitor on interstitial myofibroblast formation and matrix deposition in a nephrotic model. 960 36

It is generally accepted that hypertension and other vascular pathologies increase in diabetes mellitus (DM) patients as a result of the renin-angiotensin-aldosterone (RAA) system. In this study, changes in the renin-angiotensin-aldosterone (RAA) system level was determined in Streptozotocin (STZ)-injected rats. A total of 46 female Wistar albino rats (180-220 g body weight) was utilized in these experiments. STZ was given intraperitoneally to induce diabetes in rats. Streptozotocin (60 mg kg(-1) body weight) was dissolved in 0.1 m citrate--phosphate buffer (pH 4-5). The non-diabetic rats were injected with sterilized buffer alone to act as a control group. Blood glucose levels were 398+/-8.2 mg dl(-1), 488+/-11.75 mg dl(-1) and 658+/-29.6 mg dl(-1) at days 3, 12 and 30 respectively. The level of plasma renin activity (PRA) was measured as 7.69+/-1.07 ng ml(-1) h(-1); 1.82+/-0.22 ng ml(-1) h(-1) and 0. 67+/-0.12 ng ml(-1) h(-1) at days 3, 12 and 30, respectively. These values showed that the PRA levels are decreased with increased time period. Serum angiotensin converting enzyme (ACE, E.C. 3.4.15.1) levels were increased at days 12 and 30 (p<0.05 and p<0.005), whereas serum aldosterone levels were increased at days 3 and 12 (p<0.05). The level of urea and creatinine increased at days 12 and 30 (p<0.05 and p<0.005, respectively) when compared to the control group. The data from these experiments indicate that the PRA level decreased whereas ACE activity level increased in diabetic rats compared with the control. Aldosterone levels increased at the first stage of the experiment, but then decreased by the end of the experiment as a result of changes in renin and ACE levels.
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PMID:The study of renin-angiotensin-aldosterone in experimental diabetes mellitus. 1122 74

The effect of arsenic compounds depends on the chemical form and is specific for certain organs. The lack of specific biological indicators for the effects of each arsenic species makes it difficult to differentiate their toxicity. Five prospective biological indicators of systemic toxicity were examined at time points ranging from 15 min to 24 h using male Sprague-Dawley rats, B6C3F1 mice, Golden-Syrian hamsters, and Hartley guinea pigs, following intraperitoneal dosing with 0.1 and 1 mg/kg sodium arsenite. Rats and mice were also dosed with 1 mg/kg sodium arsenate. Total blood arsenic levels were determined in all animal species to show that exposure occurred and as an index of the severity of the change is an indicator of toxicity. Total blood arsenic levels were increased in all animal species. This increase was dose, arsenic species, and animal dependent. Renal pyruvate dehydrogenase activity was significantly decreased at early time points in mice, hamsters, and guinea pigs, and at later time points in rats dosed with arsenite. Rats and mice dosed with arsenate also exhibited PDH decrease at early time points. Blood hematocrit and glucose were increased in the rat and guinea pig, respectively, after arsenite administration. Creatinine and urea nitrogen were found to be unresponsive to arsenic in most animal species. Data suggested that the mouse and secondly the hamster appear to be the most appropriate animal models for the study of acute arsenic toxicity.
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PMID:Systemic indicators of inorganic arsenic toxicity in four animal species. 1065 39


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