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)

Nephropathy is a frequent complication of long term diabetes. Diabetic nephropathy is the major determinant of premature morbidity and mortality both in insulin-dependent (IDDM) and in non-insulin dependent-diabetes mellitus (NIDDM). There is good evidence that genetic predisposition plays a major role in development of diabetic nephropathy. This hypothesis is based on the observation that diabetic nephropathy clusters within families, both in IDDM and NIDDM. Components of the renin-angiotensin system (RAS) are plausible candidate genes to examine for a association with microalbuminuria and diabetic nephropathy. In this study we compared the distribution of PstI melting polymorphism at the ACE locus among NIDDM patients with diabetic nephropathy and in patients who, despite long duration of NIDDM, remain without this complication. The 220 NIDDM patients for whom DNA was available were classified into two groups according to their renal status: normoalbuminuric control subjects (n = 80) who are NIDDM patients with an A/C ratio < 2.5 and nephropathy cases (n = 140) who are NIDDM patients with A/C ratio > 2.5. Albumin excretion rate was assayed by radioimmunoassay. HbA1c was assayed using HPLC methods, creatinine--using Jaffe methods and DNA analysis using PCR reaction, and then after the amplification product was digested with PstI enzyme. The study revealed that PstI sequence differences ("+/= and -") in the ACE gene do not contribute to genetic susceptibility to diabetic nephropathy in NIDDM.
Pol Arch Med Wewn 1997 Jul
PMID:[Is PstI polymorphism of the angiotensin I converting enzyme gene associated with nephropathy development in non-insulin-dependent diabetes mellitus (preliminary study)]. 949 4

Hypertension is an important risk factor for vascular disease. Primary goal of hypertension treatment is to prevent or delay the onset of blood pressure-related morbidity and mortality. It has been well demonstrated that the responses rate to any single class of antihypertensive agent, give as monotherapy is approximately 45% to 55%, and in half of hypertensive population a second will be required. The data from clinical trials clearly demonstrate that two-drug combination, usually with low-dose diuretics with any one of the other first-line agents increases the response rate to about 80% to 85% and reduces the likelihood of adverse events and alteration in lipid, carbohydrate and electrolyte metabolism. Of the various combinations being given that of an diuretic and ACE inhibitor, and ACE inhibitor and non-dihydropyridine calcium channel blockers seems particularly attractive. Some combinations are inappropriate, such as diuretic and calcium channel blockers, and beta-blocker with verapamil and diltiazem. Combination of ACE inhibitor and a non-dihydropyridine calcium channel blockers may provide benefit in regression left ventricular hypertrophy diabetic nephropathy, and post myocardial infarction.
Pol Merkur Lekarski 1998 Jan
PMID:[Combination therapy in primary hypertension]. 955 8

Chronic heart failure (CHF) is present in 1-10% of the whole population. From the drugs used in CHF so far only angiotensin converting enzyme inhibitors and nitrate with hydralazine improved the survival which was caused by beneficial influence of these drugs on neurohormonal factors. There is growing interest in beta-blockers which are believed to stop the progress of CHF. Although the first attempts of using beta-blockers in the treatment of CHF took place in 70-ties, only recent years brought better understanding of mechanisms of their action. The beneficial effect of beta-blockers in CHF is related to their protective influence on myocardium and to hampering of apoptosis--programmed cell death--the phenomenon which is exaggerated in CHF. The investigations carried out in last years proved that carvedilol which is beta 1-, beta 2- and alpha 1-blocker and has antioxidant properties improved clinical status and reduced mortality in the cohorts of patients with all-cause CHF. At present great trials estimating various beta-blockers and comparing these drug among themselves are being conducted.
Pol Merkur Lekarski 1998 Jan
PMID:[Use of beta-adrenoreceptor antagonists in treatment of patients with chronic heart failure]. 955 9

This article presents a case of 45-year-old man with polycythemia vera non diagnosed before. The first symptom of polycythemia vera was acute congestive heart failure which suggested diagnosis of myocarditis. Polycythemia vera was confirmed by raised hematocrit, significantly increased platelet count, normal oxygen saturation, score for leukocyte alkaline phosphatase (LAP)-130 and splemomegaly. Echocardiography revealed left ventricular histological. Coronary arteriography showed normal coronary arteries. Finding of histological examination of the endomyocardial biopsy were described as necrosis of myocytes and abnormal blood flow in very small coronary vessels. It was the main reason of dilated cardiomyopathy caused by microinfarcts in polycythemia vera. Hematological parameters were reduced to normal levels after hydroxyurea treatment. Digitalis and ACE-inhibitor therapy quickly improved cardiovascular status from III to II NYHA class.
Pol Merkur Lekarski 1998 Jan
PMID:[A case of dilated cardiomyopathy caused by myocardial microinfarcts in the course of polycythemia vera]. 958 43

The influence of 21-day administration of captopril and enalaprilat on barium chloride and adrenaline-induced experimental arrhythmias was assessed. The experiments were performed on rabbits. Arrhythmias were evoked by two alternative arrhythmogen doses. The patterns of disturbances, their frequency and duration were evaluated on the basis of ECG examination. Antiarrhythmic properties of angiotensin converting enzyme inhibitors administered for 21 days were also compared with their effects after single administration. The results were subjected to statistic analysis. On the basis of the obtained results we were able to establish that repeated administration of enalaprilat decreases the frequency of barium chloride- and adrenaline-induced arrhythmias. Repeated administration of captopril and enalaprilat shortened the duration of adrenaline- and barium chloride-induced arrhythmias. Long-term enalaprilat administration was much more effective in preventing arrhythmias than its single dose, it also proved to be more efficient than either single or repeated administration of captopril.
Pol J Pharmacol
PMID:Evaluation of antiarrhythmic activity of captopril and enalaprilat in experimental cardiac arrhythmias in rabbits. Part II. 986 31

The present study was undertaken to investigate the influence of captopril and enalaprilat--two different angiotensin converting enzyme (ACE) inhibitors--on experimental cardiac arrhythmias induced by barium chloride, ouabain or adrenaline. The research was carried out on rabbits. Captopril and enalaprilat were administered only once. Arrhythmias were evoked by three different doses of arrhythmogens: ED50 and two higher ones causing rhythm disturbances in 80-100% rabbits. The patterns of arrhythmias as well as their frequency and duration were evaluated on the basis of ECG examination. The results were subjected to statistic analysis. As a result of our research, we were able to establish that ACE inhibitors, when administered at a single dose, did not influence the patterns but changed the frequency and duration of barium chloride-, adrenaline- or ouabain-induced arrhythmias. Captopril and enalaprilat administered at a single dose decreased the frequency of barium chloride- or ouabain- but not adrenaline-induced arrhythmia. A single administration of captopril and enalaprilat limit the duration of arrhythmias caused by barium chloride, ouabain or adrenaline.
Pol J Pharmacol
PMID:Evaluation of antiarrhythmic activity of captopril and enalaprilat in experimental cardiac arrhythmias in rabbits. Part I. 986 30

Genetic and familial factors may predispose to H-gestosis. The aim of our study was to answer the question if angiotensinogen gene m235t polymorphism, and ACE gene I/D and Pst I RFLP polymorphisms may be markers of genetic predisposition to the H-gestosis. 246 pregnant women (median age 26 years) were studied (the studied group consisted of 116 women with H-gestosis and the control group consisted of 130 healthy pregnant women). Genotyping was performed using polymerase chain reaction method. Statistical analysis was done by means of Statistica for Windows. Genotype distribution was analyzed using chi 2 test. P < 0.05 was considered as statistically significant. In our study we did not receive statistically significant differences in ACE and angiotensinogen genes genotype distributions and allele frequencies between the investigated groups. Based on results of the study we may suggest that I/D and Pst I RFLP ACE gene polymorphism and angiotensinogen gene m235t polymorphism do not play any significant role in the pathogenesis of H-gestosis.
Pol Arch Med Wewn 1998 Jul
PMID:[Lack of relationship between angiotensinogen gene m235t polymorphism and gene insertion/deletion (I/D-intron 16) and Pst I RFLP (P/M-intron 7) polymorphisms of the angiotensin I converting enzyme(ACE) gene and the development of H-gestosis. Preliminary results]. 1008 10

Congestive heart failure (CHF) is growing epidemiologic and clinical problem, and is the only common cardiovascular condition that is increasing in incidence, prevalence and mortality. During last years numerous clinical trial have been conduced evaluating the effect of various treatment procedures on clinical endpoints in patients with CHF. The major risk factor for CHF are hipertension and atherosclerotic vascular diseases, and now it is clear that aggressive treatment of hypertension and hyperlipidemia can be effective in preventing CHF. Treatment strategies for CHF are aimed at preventing and delaying progression of the disease and improving survival. In the treatment of CHF diuretics are at present the first drugs line for patients with fluid retention and are necessary to relieve symptoms but cannot halt progression or improve the prognosis of CHF. Angiotensin-converting enzyme inhibitors (ACE inhibitors) therapy has been shown to decrease mortality and progression of CHF and should be used early in patients with left ventricular dysfunction whether they have symptomatic or asymptomatic CHF. Digoxin therapy is associated with decrease in the risk of worsening CHF irrespective of rhythm, systolic function, severity of CHF or therapy with ACE inhibitors. In patients with symptomatic CHF due to systolic dysfunction the addition of diuretics and digoxin appears to reducing worsening CHF without improving survival. Other than digoxin oral inotropic agents (amrinone, pimobendan, vesnarinone, ibopamine) increase mortality in patients with CHF and have not improved symptom status and other clinical endpoints during long-term therapy. Hydralazine and isosorbide dinitrate administrated in combination are less effective alternative to ACE inhibitors. Beta-blockers and particular carvedilol may prolong survival and decrease worsening CHF when used in combination with digoxine, diuretics and ACE inhibitors. Beta-blockers therapy improve hemodynamics, LVEF and functional status patients with CHF and the ideal candidate for this therapy is stable patients with NYHA II-III CHF due to nonischemic cause. Calcium antagonists do not appear to be useful in patients with CHF, although amlodipine and mibefradil appears to be safe for treatment of angina or hypertension in this group. On the basis of current data, antiarrhythmic agents should not be given to patients with CHF free from arrhythmia but those with sustained ventricular tachycardia or ventricular fibrillation amiodaron appears to be safe.
Pol Merkur Lekarski 1999 Mar
PMID:[Trends in pharmacological treatment of congestive heart failure]. 1036 2

In the paper available information concerning the influence of treatment with angiotensin converting enzyme inhibitors (ACE-I) on cough, bronchial hyperreactivity and bronchoconstriction are reviewed. Cough occurs in 0.7% to 19% of patients treated with angiotensin converting enzyme inhibitors according to various reports. In the mechanism of angiotensin converting enzyme inhibitor-induced cough accumulation of bradykinin and substance P due to decreased degradation of this mediators caused by ACE-I may be involved. Part of tussive effect may be mediated via prostaglandins and histamine. In a few studies symptoms of airway obstruction and asthma worsening in relation to treatment with this drugs was reported. However, majority of reports suggest safety in taking ACE-I by patients with asthma. The only effective method to relieve angiotensin converting enzyme-induced cough is a drug withdrawal. The change of drugs within the whole class of ACE-I does not bring effect.
Pol Merkur Lekarski 1999 May
PMID:[Cough, bronchoconstriction and bronchial hyperreactivity in relation to treatment with angiotensin-converting enzyme]. 1043 3

Heart failure is a common and increasing public problem. Neurohormonal activation plays a role in the pathophysiology of heart failure, but is probably also affected by cytokines. We studied 75 patients with heart failure NYHA functional class II and III-IV, who were treated with angiotensin converting enzyme inhibitor (enarenal), diuretics (furosemide) and digoxine. Their mean age was 63.9 years/range 65-86/, left ventricular ejection fraction in the patients NYHA functional class II and III-IV classes was 68.9% and 47.3% respectively; 12 were females. Significant improvements in NYHA classification were shown. The levels plasma TNF-alpha (tumor necrosis factor-alpha) and interleukin-6 (IL-6) were analysed before and after therapy. The authors showed increased plasma levels TNF-alpha and IL-6 in patients with chronic heart failure. After the treatment the plasma IL-6 levels decreased only in the patients III-IV NYHA functional classes, whereas the treatment had no effect on the plasma TNF-alpha levels.
Pol Merkur Lekarski 1999 Aug
PMID:[Do cytokines have any value in the patients with chronic blood circulation insufficiency?]. 1052 13


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