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)

The effects of trandolapril (0.25 mg/kg body wt per 48 hours) on aortic atherosclerosis were examined in the Watanabe heritable hyperlipidemic rabbit treated from 3 to 12 months of age. Trandolapril caused a significant decrease in atherosclerotic involvement of the intimal surface of total aorta from 56.3 +/- 5.0% in control Watanabe rabbits to 35.0 +/- 4.1% with treatment (p less than 0.01). The largest reductions were observed in descending thoracic aorta where 21.8 +/- 5.7% of intimal surface was involved in the trandolapril-treated animals versus 54.4 +/- 7.7% in the control group (p less than 0.01). Significant decreases also occurred in ascending aorta/arch and abdominal aortic segments. Cholesterol content of descending thoracic aorta was also significantly reduced in the trandolapril-treated rabbits. The atherosclerotic plaques in aorta from trandolapril-treated rabbits appeared to contain less foam cells and relatively greater amounts of connective tissue than those from control animals. These studies indicate that trandolapril inhibits aortic atherosclerosis in the Watanabe heritable hyperlipidemic rabbit. The similarity in results between the current study and that using captopril suggests that the antiatherosclerotic action of trandolapril and captopril represents a class effect related to angiotensin converting enzyme inhibition.
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PMID:Trandolapril inhibits atherosclerosis in the Watanabe heritable hyperlipidemic rabbit. 139 82

Although the pathology of essential hypertension is still unclear, studies have shown that doxazosin, a selective alpha 1-inhibitor, is able to effectively control mild-to-moderate hypertension. The aim of these two, noncomparative studies was to evaluate the efficacy and toleration of doxazosin when used as monotherapy and in combination with other antihypertensive agents. In study I, 154 patients with standing and sitting diastolic blood pressures (DBPs) ranging from 95 to 115 mm Hg were treated with once-daily doxazosin (1 to 8 mg) as monotherapy for 12 weeks. Both sitting and standing blood pressures were significantly reduced by doxazosin monotherapy. Target DBP of less than or equal to 90 mm Hg was achieved in 86% of patients after 12 weeks of therapy with doxazosin, and there was no change in heart rate. Cholesterol and triglyceride levels were significantly decreased by doxazosin, but there was no change in glucose levels. Minor side effects were seen in 17.5% of patients, and 2.6% discontinued therapy. In study II, 65 patients with DBPs ranging from 95 to 115 mm Hg on existing antihypertensive therapies were concomitantly treated with doxazosin (1 to 8 mg) once daily for 12 weeks. Target DBPs of less than or equal to 90 mm Hg was achieved in 71% of patients after 12 weeks of therapy with doxazosin. There was no change in heart rate throughout the treatment period, and plasma cholesterol, triglyceride, and glucose levels remained essentially unchanged. Three patients, each receiving a beta-blocker, a diuretic, and doxazosin, were withdrawn because of side effects. Minor side effects, which were considered drug related were seen in 21% of patients. Doxazosin is a drug with good antihypertensive efficacy and is well tolerated as monotherapy and in combination with beta-blockers, thiazide diuretics, angiotensin converting enzyme inhibitors, and various combinations of these drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Control of coronary heart disease risk factors with doxazosin as monotherapy and in combination therapy. 290 47

Ninety-four normotensive type II diabetics with normal renal function and microalbuminuria were randomized to receive enalapril 10 mg/day or placebo and were followed for five years. In the patients treated by enalapril plasma creatinine values and albuminuria remained stable throughout the observation period. Their plasma total cholesterol decreased from an initial value of 245 +/- 27 mg/dl to mean study value of 236 +/- 29 mg/dl, and to a fifth year value of 232 +/- 27 mg/dl (P < 0.001). The changes in HDL cholesterol and triglyceride values were nonsignificant. In the placebo group there was a significant increase in albuminuria and a mean decline of 13% in reciprocal creatinine values during the five years. Plasma total cholesterol increased from an initial mean value of 246 +/- 24 to a mean study value of 252 +/- 25 mg/dl, and to a fifth year mean value of 259 +/- 32 mg/dl (P < 0.001). There was a significant correlation between both initial and mean plasma total cholesterol values, and the decline in renal function and the rise in albuminuria in the placebo treated patients. This correlation persisted after stratification for blood pressure. Treatment with enalapril did not eliminate these correlations. Cholesterol may be an additional risk factor for diabetic nephropathy. ACE inhibitors may have a modest cholesterol lowering effect in diabetic patients mediated, in part, through the decline in albuminuria.
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PMID:Plasma lipids and the progression of nephropathy in diabetes mellitus type II: effect of ACE inhibitors. 775 91

About one hundred European cardiologists discussed the role of calcium antagonists in the follow-up management of myocardial infarction. beta-blockers are the treatment of choice. Where these are contra-indicated or otherwise unsuitable, many clinicians would use a non-dihydropyridine calcium antagonist alone or in combination with an ACE inhibitor. There is broad agreement that calcium antagonists should not be used in patients with concomitant left ventricular failure. Cholesterol estimation in post-infarction patients is essential.
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PMID:How European cardiologists perceive the role of calcium antagonists in follow-up after myocardial infarction. 904 49

During acute myocardial infarction (MI), aspirin, beta-adrenergic antagonists and oral angiotensin converting enzyme (ACE) inhibitors should be used as an adjunct to reperfusion therapy. Medications upon discharge from the hospital should include aspirin and a beta-blocker. An ACE inhibitor should also be prescribed unless the ejection fraction is > 45%. Particular indications for an ACE inhibitor are an anterior MI, congestive heart failure, ejection fraction < 45% and mitral regurgitation. beta-blockers, when given to patients treated with ACE inhibitors, appear to produce an additional benefit compared with an ACE inhibitor alone. Based on the Scandinavian Simvastatin Survival Study (4S), Cholesterol and Recurrent Events (CARE) and Long-Term Intervention with Pravastatin in Ischemic Disease (LIPID) trials, a statin should also be given to subjects with low density lipoprotein (LDL)-cholesterol levels above 125 mg/dl, independent of total cholesterol levels. Therapy should be administered in an attempt to reduce the LDL-cholesterol level to 90-100 mg/dl (2.3-2.6 mM/l). In patients with normal or low levels on initial evaluation, screening for lipid abnormalities should be deferred for 2 months since acute phase responses and passive hepatic congestion can cause spuriously normal levels. Calcium channel blockers, nitrates, lidocaine, anti-arrhythmic drugs and i.v. magnesium should not be administered routinely after acute MI and their use should be restricted to selected settings.
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PMID:Modern adjunctive pharmacotherapy of myocardial infarction. 1124 26

Whether hormone replacement therapy (HRT) is beneficial for coronary heart disease (CHD) is controversial. We hypothesized that continuous combined transdermal HRT may have benefits on CHD risk markers without the potential adverse effects seen with certain other HRT regimens. Sixty apparently healthy postmenopausal women, aged 40-65 years, entered a prospective, double-blind, randomized, placebo-controlled clinical trial; 55 women completed the 6-month study. Women received either transdermal oestradiol 17beta 0.05 mg and norethisterone acetate 0.125 mg daily, or identical placebo. Circulating markers of vascular function and remodelling, forearm blood flow, lipids and lipoproteins, glucose and insulin, and haemostatic safety parameters were measured at baseline and after treatment. Compared with placebo after 6 months, HRT administration resulted in decreased E-selectin (P < 0.01), and angiotensin-converting-enzyme (ACE; P = 0.05). Cholesterol (P < 0.05), low-density lipoproteins (LDL; P < 0.05), high-density lipoprotein3 (HDL3; P < 0.05) and apolipoproteins AII (P < 0.05) and B (P < 0.05), and fasting insulin (P < 0.05) also decreased in the HRT group. Factor VII coagulation activity decreased (P < 0.01) and plasminogen activator inhibitor-1 and fibrin D-dimer increased (P < 0.05) in the HRT group, whilst prothrombin fragment 1 + 2 (P < 0.05) decreased, more so in the placebo group. There were no changes in matrix metalloproteinase (MMP)-2, or in LDL particle size. This transdermal HRT had beneficial effects on vascular function and CHD risk markers.
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PMID:Randomized trial of effect of transdermal continuous combined hormone replacement therapy on cardiovascular risk markers. 1500 73

The metabolic syndrome is intended to identify patients who have increased risk of diabetes and/or a cardiac event due to the deleterious effects of weight gain, sedentary lifestyle, and/or an atherogenic diet. The National Cholesterol Education Program's Adult Treatment Panel III definition uses easily measured clinical findings of increased abdominal circumference, elevated triglycerides, low high-density lipoprotein-cholesterol, elevated fasting blood glucose and/or elevated blood pressure. Three of these five are required for diagnosis. The authors also note that other definitions of metabolic syndrome focus more on insulin resistance and its key role in this syndrome. This review focuses on how treatment might affect each of the five components. Abdominal obesity can be treated with a variety of lower calorie diets along with regular exercise. Indeed, all of the five components of the metabolic syndrome are improved by even modest amounts of weight loss achieved with diet and exercise. For those with impaired fasting glucose tolerance, there is good evidence that a high fiber, low saturated fat diet with increased daily exercise can reduce the incidence of diabetes by almost 60%. Of note, subjects who exercise the most, gain the most benefit. Metformin has also been shown to be helpful in these subjects. Thiazolidinedione drugs may prove useful, but further studies are needed. Although intensified therapeutic lifestyle change will help the abnormal lipid profile, some patients may require drug therapy. This review also discusses the use of statins, fibrates, and niacin. Likewise, while hypertension in the metabolic syndrome benefits from therapeutic lifestyle change, physicians should also consider angiotensin converting enzyme inhibitor drugs or angiotensin receptor blockers, due to their effects on preventing complications of diabetes, such as progression of diabetic nephropathy and due to their effects on regression of left ventricular hypertrophy. Aspirin should be considered in those with at least a 10% risk of a coronary event over 10 years. Finally, three related conditions, nonalcoholic fatty liver disease, polycystic ovary syndrome and protease inhibitor associated lipodystrophy improve with therapeutic lifestyle change. Although metformin is shown to be useful with polycystic ovary syndrome, the data supporting drug therapy for the other syndromes is less convincing. More robust studies are needed before any firm recommendations can be made.
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PMID:Treatment of metabolic syndrome. 1515 70

We have investigated the frequencies of seven markers among 100 unrelated individuals with angiographically documented CAD (Coronary Artery Disease) and among 100 unrelated healthy blood donors in the central region of Corsica island (France). The seven polymorphisms analyzed were chosen from six candidate genes involved in (1) Renin-Angiotensin system: Angiotensin converting enzyme (ACE I/D), (2) Lipid metabolism: Cholesterol Ester Transfer Protein gene (CETP TAQ1B), (3) Platelet aggregation: alpha and beta subunits of the platelet GpIIb/GpIIIa integrin complex (GpIIb HPA3 and GpIIIa Pl(A1/A2)), (4) Coagulation fibrinolysis: Plasminogen Activator Tissue (PLAT TPA25 I/D) and Methylenetetrahydrofolate Reductase (MTHFR C677T and A1298C). The samples were genotyped using the polymerase chain reaction followed by restriction enzyme analysis for the RFLPs. No significant difference in allele frequencies between patient and control groups was observed. The occurrence of the MTHFR T677T genotype and of the T677T/A1298A compound genotype is higher in cases (20%) than in the controls (4%). Odds ratio seems to indicate that individuals with the MTHFR T677T genotype and the T677T/A1298A compound genotype had a 6-fold increased risk for developing CAD (ORs = 6; 95% CIs = 1.96-18.28) suggesting a possible association of MTHFR C677T with the risk of CAD in Corsican population.
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PMID:Prevalence of genetic risk factors for coronary artery disease in Corsica island (France). 1624 96

Insulinresistance is a component of the metabolic syndrome and important pathogenetic factor of type 2 diabetes mellitus. There are evidences that activation of the renin-angiotensin system (RAS) can decrease insulin sensitivity of tissues. As I/D polymorphism of angiotensin converting enzyme (ACE) gene can influence the activity of RAS, it may also influence insulin resistance. Aim. To assess the relationship between the I/D polymorphism of ACE gene and degree of insulin resistance and intensity of metabolic syndrome in type 2 diabetic patients. Study group and methods. Examined group: 108 type 2 diabetic patients (38 women and 70 men), with mean duration of disease 9.07 +/- 6.68 years, mean age 59.98 +/- 9.10 years. Assessed parameters: body mass index (BMI), waist/hip ratio (WHR), arterial blood pressure. Laboratory tests: concentration of the glycosylated hemoglobin (HbA 1c), glucose, insulin, total cholesterol, HDL and LDL cholesterol, triglycerides, creatinine, uric acid. Insulin resistance was calculated by the HOMA rate. Criterion of insulin resistance was rate > or = 2.5. The diagnosis and assessment of intensity of metabolic syndrome was performed according to criteria of National Education Cholesterol Adult Treatment Program the Panel III. I/D ACE gene polymorphism was evaluated by polymerase chain reaction (PCR). Results. Groups with 11, ID and DD genotype were not different in age, BMI, WHR, duration of diabetes, the prevalence and duration of arterial hypertension, degree of metabolic control and insulinresistance assessed by HOMA rate and intensity of metabolic syndrome. DD genotype carriers had significant higher systolic and diastolic blood pressure (147.8 +/- 19.8 mmHg vs 138.2 +/- 16.5 mmHg, p = 0,02; 89.2 +/- 9.6 mmHg vs 81.7 +/- 8.6, p = 0,003, respectively) than II patients. Conclusion. In type 2 diabetic patients the I/D genotype of ACE gene is not associated with the increased insulin resistance assessed by HOMA rate and intensity of metabolic syndrome.
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PMID:[I/D polymorphism of angiotensin I converting enzyme gene and insulin resistance and some parameters of metabolic syndrome in patients with type 2 diabetes]. 1678 86

Metabolic Syndrome (MS) is recognized as a cluster of cardiovascular risk factors. All components of MS have a genetic base. Genes of the renin angiotensin system are potential candidate genes for MS. We investigated whether angiotensin converting enzyme (ACE) gene polymorphism increases susceptibility to MS as an entity in a Mexican population. In a cross-sectional study, 514 individuals were studied including 245 patients with MS and 269 subjects without MS criteria. ACE gene polymorphism was detected using PCR. MS was defined according to The National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) criteria, except that the raised fasting plasma glucose <or=100 mg/dl criterion for identification of intolerance fasting glucose was modified in accordance with the suggestion of the American Diabetes Association. Patients with MS were significantly different from subjects without MS in relation to mean body mass index (BMI), waist circumference (WC), systolic blood pressure, diastolic blood pressure, glucose, total cholesterol (C), triglycerides, HDL-C, and LDL-C (P<0.0001). The differences in the mean BMI, WC, glucose, total cholesterol, triglycerides, LDL-C, and HDL-C were maintained in patients with the MS and DD genotypes (P<0.01). The DD genotype was strongly associated with MS (adjusted OR=5.48, 95% CI 3.20-9.38, P<0.0001). We concluded that the DD genotype increases susceptibility to MS in a Mexican population. These results indicate that pharmacological and non-pharmacological treatment and a reduction in body fat will have important therapeutic implications in this disease.
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PMID:Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population. 1760 86


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