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 goal of the current study was to determine whether treatment of hypertension reduces cerebral infarction after occlusion of the middle cerebral artery in stroke-prone spontaneously hypertensive rats (SHRSPs). Three-month-old SHRSPs received untreated drinking water or drinking water containing cilazapril, an angiotensin converting enzyme inhibitor, or hydralazine and hydrochlorothiazide. After 3 months of treatment, the left middle cerebral artery was occluded and neurological deficit was evaluated. Infarct volume was measured 3 days after occlusion using computer imaging techniques from brain slices. Cilazapril and hydralazine with hydrochlorothiazide were equally effective in reducing systolic blood pressure in SHRSPs. One day after occlusion of the middle cerebral artery, neurological deficit was decreased by both cilazapril and hydralazine with hydrochlorothiazide compared with untreated SHRSPs, and the deficit 3 days after occlusion was decreased significantly only by cilazapril. Infarct volume was 178 +/- 7 mm3 (mean +/- SEM) in untreated SHRSPs, and it was significantly reduced to 117 +/- 15 mm3 by hydralazine with hydrochlorothiazide and to 101 +/- 17 mm3 by cilazapril. Infarct volume in Wistar-Kyoto rats was 27 +/- 16 mm3. Thus, reduction in arterial pressure by hydralazine with hydrochlorothiazide or an angiotensin converting enzyme inhibitor is protective against focal cerebral ischemia in SHRSPs.
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PMID:Effect of antihypertensive treatment on focal cerebral infarction. 153 16

Since hypertension is an important risk factor for atherosclerosis, it is logical to assume that treatment to lower blood pressure will prevent atherosclerosis. However, the relationship between hypertension and atherosclerosis is indirect and complex. Drugs that lower pressure will prevent heart failure and arteriolar complications such as renal failure or strokes caused by lacunar infarction or brain haemorrhage due to rupture of microaneurysms. However, there is little evidence that atherosclerotic complications can be reduced by lowering pressure. It is important to understand the pathogenesis of atherosclerosis and its complications, which are related to lipoproteins and arterial flow disturbances, in order to develop an approach to selecting those antihypertensive drugs which may prevent atherosclerotic complications related not only to initiation and progression of atherosclerotic plaques, but to the embolisation of platelet clumps or atherosclerotic debris, or events such as intraplaque haemorrhages, that lead to myocardial or cerebral infarction. Antihypertensive drugs have different effects on lipoproteins and on arterial flow disturbances that may have important implications for prevention. Alpha-blockers and drugs with beta 2 agonist activity have beneficial effects on lipoprotein profiles, ACE inhibitors and calcium channel antagonists have some anti-atherosclerotic effects in animal models, while beta-blockers have beneficial effects on flow disturbances and are anti-atherosclerotic in animal models and man. Future studies to determine how to prevent atherosclerotic complications in hypertensive patients will require methods for noninvasive measurement of atherosclerosis.
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PMID:Pathogenesis of atherosclerosis and its complications: effects of antihypertensive drugs. 269 95

Criteria for the diagnosis of exercise hypertension have not yet been established. Published values for blood pressure increase during dynamic exercise in normotensive healthy persons differ greatly dependent on age, sex, heart frequency and load of dynamic exercise. Upper normal systolic values during exercise reach levels between 200 and 230 mm Hg. The incidence of exercise hypertension is therefore reported to range from 1 to 10% of the total population. Follow-up studies show that 10 to 60% of persons with isolated exercise hypertension proceed to chronic arterial hypertension. No results are available on exercise hypertension as a risk factor in contrast to the well-known link between increased systolic and diastolic casual blood pressure and cardiovascular diseases. The development of left-ventricular hypertrophy depends mainly on the average systolic blood pressure during a 24-hour period. Peak values of systolic blood pressure during the day or blood pressure variability are less important. Drug treatment of isolated exercise hypertension is not generally accepted. Non-drug treatment is to be preferred, e.g. weight reduction in overweight, dietary sodium restriction and endurance training. Drug treatment must be considered, if non-drug treatment is unsuccessful and/or risk factors, for example hypercholesterolemia, diabetes, cigarette smoking, or complications of target organs, i.e. coronary heart disease or cerebral infarction, do exist. In antihypertensive treatment of increased exercise blood pressure, the influence of the drugs on the hemodynamic and metabolic parameters must be observed, especially in patients with concomitant coronary heart disease. Increases in blood pressure due to dynamic exercise are better attenuated by antihypertensive drugs than those caused by isometric exercise. The drugs of choice are beta-blockers, preferably beta 1-blockers without ISA. Alternatively, calcium antagonists of the verapamil-type or ACE-inhibitors may be used. In contrast to other antihypertensive drugs, labetalol, calcium antagonists and ACE-inhibitors have no influence on the exercise-induced increase of cardiac index and therefore little effect on the work capacity of the circulatory system.
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PMID:[Differential therapy of exercise hypertension]. 358 8

The homozygous deletion allele of the angiotensin converting enzyme gene (ACE/DD), homozygous threonine allele of the angiotensinogen gene (AGN/TT), and the epsilon4 allele of the apolipoprotein E gene (apoE/epsilon4) are reported to be associated with ischemic heart disease. Cerebrovascular disease (CVD) is another atherosclerotic disease; and the effects of these polymorphisms on CVD have been confusing. In this study, we investigated whether ACE/DD, AGN/TT, and apoE/epsilon4 genotypes are associated with CVD and whether genetic risk is enhanced by the effect of one upon another. We ascertained these genotypes in patients with cerebral infarction (n = 55) and cerebral hemorrhage (n = 38), diagnosed by brain computed tomography. Control subjects for the infarction group and the hemorrhage group were randomly selected from 583 subjects matched for age, gender, and history of hypertension with patients. Frequency of ACE/DD genotype was higher in the patients with infarction than in the controls (chi2 = 6.1, P < .05). The AGN/TT genotype was not associated with either infarction or hemorrhage, but it increased the relative risk for cerebral infarction in the subjects with ACE/DD genotype (chi2 = 8.0, P < .01, odds ratio; 11.7, 95% confidence intervals: 1.4 to 96.0). There was no significant association between apoE/epsilon4 and CVD. These results suggest that ACE/DD predicts cerebral infarction, but not cerebral hemorrhage, and that AGN/TT enhances the risk for cerebral infarction associated with ACE/DD.
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PMID:Polymorphism of angiotensin converting enzyme, angiotensinogen, and apolipoprotein E genes in a Japanese population with cerebrovascular disease. 944 75

The aim of this study was to identify the similitudes and the differences in the epidemiology and prevention of myocardial infarction and cerebrovascular accidents by analysis of trials of primary and secondary prevention of myocardial infarction and cerebrovascular accidents. The principal risk factors common to both pathologies are hypertension, smoking and increased LDL-cholesterol. However, the statistical significance with respect to causality differs from one pathology to the other. Similarly, the impact of preventive measures is not the same: the treatment of hypertension is more important in the prevention of cerebrovascular accidents than myocardial infarction; the situation is the other way around with respect to the treatment of hypercholesterolaemia. Of the therapeutic interventions, aspirin is effective in all stages of coronary artery disease but does not prevent cerebrovascular accidents in patients without documented atherosclerosis. Thrombolysis carries a much higher benefit/risk ratio in the treatment of myocardial infarction than in that of cerebral infarction. The so-called cardioprotective drugs, such as the betablockers and angiotensin converting enzyme inhibitors, have only been used to any extent in the secondary prevention of myocardial infarction. These differences reflect the fact that cerebrovascular accident covers a range of diseases much more diverse than does myocardial infarction, and also that the brain is much more exposed to haemorrhage whereas cardiac haematoma is highly unusual. Finally, cerebral atherosclerosis is a later event than coronary atherosclerosis and this has epidemiological implications which are difficult to assess. In conclusion, the prevention of myocardial infarction and of cerebrovascular accidents may proceed theoretically by a common pathway but in practice, it is very different.
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PMID:[Heart and brain: are the risk factors the same? Are the results of primary and secondary trials comparable?]. 983 81

Several studies confirm cognitive impairment and dementia to be increased after stroke in the elderly. Although not necessarily involving memory deficits, the frequency of cognitive impairments may occur in up to 30% of stroke survivors at 3 months. This impairment may be confounded by preexisting cognitive decline or dementia. By contrast, cognitive changes and dementia are widely recognized in familial forms of stroke, such as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Several factors, including type of stroke, recurrent episodes, the site and laterality of the lesion(s), volume of cerebral infarction, medial temporal lobe atrophy, and coexistent neurodegenerative pathology predict the degree of impairment. Aphasia, diabetes mellitus, atrial fibrillation, and depression are listed among other biologic factors that further exacerbate cognition and affect long-term survival. There is no clear consensus whether genetic factors, such as the apolipoprotein E e4 allele or angiotensin converting enzyme gene polymorphisms, modify cognitive changes or stroke outcome. Although several neurotransmitter systems may be affected in post-stroke dementia, the amelioration of cholinergic function is a worthy target.
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PMID:Stroke and cognition. 1138

Insulin resistance and hyperinsulinemia have been observed in over 70% of the nonobese, nondiabetic subjects with essential hypertension (HT). Alpha-1 blockers, ACE-antagonists, long-acting Ca blockers including nifedipine CR, some form of beta-blockers, tilisolor, which is reported to increase blood flow, improve insulin sensitivity when blood pressure is better controlled. Decrease of serum potassium during insulin sensitivity test and intraplatelet free Ca2+ concentration is positively and negatively correlated with insulin sensitivity, respectively. Blood pressure is correlated with insulin resistance, which is also observed in secondary HT. The resistance is correlated with salt sensitivity as well as impaired nocturnal fall of blood pressure. These suggest the possible association of insulin resistance with altered intracellular cation metabolism. Insulin resistance and associated hyperinsulinemia have been observed in effort as well as vasospastic angina pectoris (VSAP), atherothrombotic cerebral infarction, and in ASO without obesity, HT, or diabetes, suggesting the resistance resulting from endothelial dysfunction. Insulin resistance has been observed in heart failure and is correlated with angiotensin II. Resistance is also observed in hypertrophic cardiomyopathy and is partially correlated with TNF-alpha. These results indicate that insulin resistance seem to be multifactorial. An effort to normalize insulin sensitivity is crucial to eliminate multiple risk factors as well as to prevent the progression of atherosclerotic vascular lesions.
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PMID:Multifactorial insulin resistance and clinical impact in hypertension and cardiovascular diseases. 1187 61

Diabetic patients have a higher incidence of stroke, especially cerebral infarction. Hypertension as well as aging and sex differences are recognized as a major factor for stroke. In addition, diabetes is likely to be accompanied by hypertension. Recently, many mega studies have reported that aggressive blood pressure reduction significantly reduced stroke. Therefore, the tighter control of blood pressure is required to prevent stroke in diabetic patients as compared with non-diabetic subjects. Desirable target pressure is less than 130/80 mmHg and the treatment in older patients should be almost the same as in younger patients, although blood reduction should be attempted safely and by a step. The use of ACE-inhibitor and/or Ca antagonist is recommended as first-line drugs for achieving it.
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PMID:[Cerebrovascular disease and diabetic patients with hypertension]. 1287 81

The homozygous deletion allele of the angiotensin-converting enzyme gene (ACE/DD), homozygous threonine allele of the angiotensinogen gene (AGN/TT), and the epsilon4 allele of the apolipoprotein E gene (apoE/epsilon4) are reported to be associated with ischemic heart disease. Cerebral infarction (CI) is another atherosclerotic disease, and the effects of these polymorphisms on CI have been confusing. The frequency of the DD genotype of the ACE gene, but not the TT genotype of the AGN gene and the epsilon4 allele of ApoE, was significantly higher in subjects with than those without CI in Japan. In this study, we investigated whether ACE/DD, AGN/TT, and apoE/epsilon4 genotypes are associated with CI and whether genetic risk is enhanced by the effect of one upon another. We ascertained these genotypes in patients with CI (n = 365), diagnosed by brain computed tomography. Control subjects for the infarction group were randomly selected from 319 subjects matched for age, gender, and history of hypertension with patients. The ACE/DD genotype was not associated with CI. Frequency of the AGN/TT genotype was higher in patients with CI than in controls (chi2 = 12.287, p < 0.05). The frequency of t allele was 0.88 in patients and 0.82 in controls (chi2 = 11.041, p < 0.05; odds ratio, 1.7). Furthermore, the AGN/TT genotype increased the relative risk for CI in subjects with the ACE/DD genotype (chi2 = 7.8, p < 0.05; odds ratio, 1.9). There was no significant association between apoE/epsilon4 and CI. These results suggest that AGN/TT predicts CI and ACE/DD enhances the risk for CI associated with AGN/TT in a Korean population.
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PMID:Polymorphism of angiotensin-converting enzyme, angiotensinogen, and apolipoprotein E genes in Korean patients with cerebral infarction. 1450 Sep 90

Sasang constitutional medicine is a major branch of Korean traditional oriental medicine. Constitutions of Sasang medicine refer to Taeyangin, Taeumin, Soyangin, and Soumin. The differences of disease severity to be shown in the constitution may be due to genetic factors. Therefore, we examined interrelationship among cerebral infarction, CI, angiotensin converting enzyme (ACE) gene polymorphism, and Sasang constitutional classification. We investigated the association between ACE genotype and CI by case-control study in a Korean population. We also classified CI patients and control group into groups according to Sasang constitutional medicine. 208 CI patients and 643 controls without CI were examined. ACE genotype was determined by 7.5 % polyacrylamide gel separation after DNA amplification. The ACE/DD genotype was not associated with CI. The frequency of Taeumin of Sasang constitutional medicine in patients with CI was significantly higher than that in controls (chi2=41.202, p<0.001). However, the Taeumin constitution did not enhance the relative risk for CI in the subjects with ACE/DD genotype. Although we did not find any association between ACE gene polymorphism and CI in Koreans, there were significant differences in allele frequencies between Koreans and Europeans, but not Japanese and Chinese populations. Furthermore, we first attempted to evaluate the efficacy of Sasang constitutional medicine, and to find an association with CI.
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PMID:Angiotensin converting enzyme gene polymorphism and traditional Sasang classification in Koreans with cerebral infarction. 1464 79


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