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)

1. We have used 125I-labelled fibrinogen (I-FN) in experiments monitoring plasma extravasation from vessels within guinea-pig trachea and peripheral lung tissue in response to platelet activating factor (PAF) and bradykinin (BK). Retained tissue radioactivity derived from I-FN was detected by direct measurement and by autoradiography. 2. Both PAF and BK caused concentration-dependent increases in radioactivity in trachea and peripheral lung, with PAF being approximately 1000 times more potent than BK at both sites. On a wet weight basis, mean tracheal leakage responses to PAF and BK were approximately 6 times and 2 times greater respectively than those in peripheral lung. Furthermore, in trachea, the maximal response to PAF was nearly twice that to BK, although they were approximately equiactive in peripheral lung. The dipeptidyl carboxypeptidase inhibitor, enalapril (1 mg kg-1, i.v.), increased the potency of BK by approximately 40 fold. 3. In trachea, PAF (50 ng kg-1, i.v.)-induced leakage was selectively inhibited by the PAF receptor antagonist, WEB 2086 (5-50 micrograms kg-1), while responses to BK (50 micrograms kg-1, i.v.) were selectively inhibited by the BK2 receptor antagonist NPC 349 (0.5-1 mg kg-1). Neither PAF nor BK-induced leakage were significantly altered by pretreatment with the histamine H1-receptor antagonists mepyramine (10 micrograms kg-1) or ketotifen (50 micrograms kg-1) or the leukotriene receptor antagonist SKF 104353. These data indicate that both agonists caused direct, specific receptor operated increases in tracheal vascular permeability to plasma macromolecules.The alpha/beta1-adrenoceptor agonist adrenaline (100 pgkg-1) caused modest inhibition of leakage induced by BK, but not of the leakage response to PAF.4. Peripheral airway leakage responses to both PAF and BK were also detected by light microscopic autoradiography in paraffin-embedded tissue sections. This was possible since a significant amount of extravasated I-FN was apparently precipitated and fixed in the extravascular space as 125-labelled fibrin. Autoradiograms showed that both agonists caused increases in peripheral bronchial circulation microvascular permeability to I-FN. No evidence for leakage in alveolar wall capillaries or in pulmonary blood vessels was observed. Quantitation of such autoradiographic data will allow a comprehensive evaluation of the effects of putative asthma mediators on microvascular permeability throughout the respiratory tree.
Br J Pharmacol 1991 Sep
PMID:Quantitative assessment of increased airway microvascular permeability to 125I-labelled plasma fibrinogen induced by platelet activating factor and bradykinin. 166 58

Sarcoidosis resolves spontaneously in many cases on a long-term basis. However, there are many cases whose resolution is delayed. We have experienced a frequent association of chronic tonsillitis (CTL), and dental caries in those patients of persistent course. We hypothesized that the presence of chronic or recurrent inflammatory foci in the upper airway may adversely affect the natural resolution of sarcoidosis. We analyzed the difference of regression of bilateral hilar lymphadenopathy on chest roentgenogram (CXR) in relation to changes in serum angiotensin converting enzyme (SACE) in sarcoidosis patients with and without CTL, and the effect of tonsillectomy (TLT) on the clinical course. In this study, we focused only on the tonsil for the sake of simplicity of analysis. Sarcoidosis resolved spontaneously in 10 of 28 (36%) patients with CTL and in 19 of 25 (76%) without CTL, and after TLT 9 cases became favorable in the course and the rate of unfavorable turned similar to those without CTL. The presence of CTL may be adversely related to the resolution of sarcoidosis.
Sarcoidosis 1991 Sep
PMID:Adverse effect of chronic tonsillitis on clinical course of sarcoidosis. 166 76

In its pulmonary form, sarcoidosis generally resolves spontaneously, but it may lead to fibrosis of the lung. The clinical, radiological and functional tests, as well as activity markers such as the serum angiotensin converting enzyme, intrathoracic uptake of 67Gallium and the cytological data provided by bronchoalveolar lavage are only the expressions at any given time of a disease which is constantly progressing and only partly express its evolutive potential. The authors studied the distribution of T-lymphocyte subsets in the peripheral blood and from bronchoalveolar lavage. 32 patients were included in the study. They were suffering from acute or chronic sarcoidosis of the mediastinum and lungs and were divided into 2 groups according to clinical, radiological and pulmonary function criteria; Group A (n = 19) included regressive forms (minimum follow up 2 years) and group B (n = 13) the progressive untreated forms. Lymphopenia with a decrease in the percentage of CD3 cells was found in both groups. The percentage of CD4 cells is significantly lower in group B (28 +/- 11%) than in group A (45 +/- 8%) (p < 0.01) or in the control population (46 +/- 8%) (p < 0.01). The percentage of CD8 cells is higher in group B (30 +/- 8%) than in group A (18 +/- 6%). This results in a CD4/CD8 ratio which is significantly reduced in group B (1 +/- 0.5) when compared with group A (2.72 +/- 0.8) (p < 0.01) and the control group (2.17 +/- 0.8) (p < 0.01), the difference between group A and the controls being minimal.(ABSTRACT TRUNCATED AT 250 WORDS)
Sarcoidosis 1991 Sep
PMID:Does peripheral blood T-lymphocyte population distribution in sarcoidosis provide a prognostic clue? 166 78

Two patients with history of intravenous drug use and pulmonary talc granulomatosis are presented. The first patient is a black female who was found to have increased activity of serum angiotensin converting enzyme, in addition to other clinical manifestations of sarcoidosis. The second patient is a Hispanic male smoker who presented with a solitary lung nodule and underwent transbronchial biopsies on two separate occasions with the diagnosis of talc granulomatosis. The lung nodule was found to be an adenocarcinoma on resection. Both patients had lung functions consistent with obstructive airways disease.
Sarcoidosis 1991 Sep
PMID:Talc granulomatosis: two unusual presentations. 166 80

ACE, a carboxypeptidase that hydrolyses angiotensin-1 to angiotensin-2, is widely found in human tissues including vascular endothelium. It is also produced by epithelioid cells of sarcoid granulomata which elevate serum ACE, a useful test of active sarcoidosis, despite its less than optimal sensitivity and specificity. It is not known why ACE production is increased in only certain granulomatous disorders. The explanation may assist our understanding of the pathogenesis of sarcoidosis.
Sarcoidosis 1991 Sep
PMID:A review of angiotensin converting enzyme in health and disease. 167 5

The content of membrane peptidases has been compared in the human astrocytoma clone D384 and the human neuroblastoma line SH-SY5Y. Endopeptidase-24.11 (neutral endopeptidase, EC 3.4.24.11) was detectable only on the astrocytoma cells whereas angiotensin-converting enzyme (EC 3.4.15.1) was selectively expressed on the neuroblastoma line. Dipeptidyl peptidase IV (EC 3.4.14.5) was also abundant on the astrocytoma line. The presence of both endopeptidase-24.11 and dipeptidyl peptidase IV on D384 cells was confirmed by immunohistochemistry. A membrane preparation from D384 cells hydrolyzed both atrial natriuretic peptide and brain natriuretic peptide and, in both cases, the pattern of metabolism was similar to that seen with purified endopeptidase-24.11. The endopeptidase-24.11 inhibitor, phosphoramidon, at 1 microM abolished natriuretic peptide metabolism. The neuroblastoma line, which lacked endopeptidase-24.11, failed to metabolise atrial natriuretic peptide and brain natriuretic peptide, emphasizing the key role of the endopeptidase in hydrolyzing these regulatory peptides at the cell surface.
Neuroendocrinology 1991 Sep
PMID:Hydrolysis of atrial and brain natriuretic peptides by the human astrocytoma clone D384 and the neuroblastoma line SH-SY5Y. 168 34

The three approaches (physiopathological, epidemiological and pharmacological) to the management of hypertension should converge to provide a personalized prescription of the most appropriate treatment to prevent and/or cure the cardiovascular complications of hypertension: hypertensive left ventricular hypertrophy and the risks directly related to it (haemodynamic, arrhythmic, ischaemic) may be corrected by certain antihypertensive agents (methyldopa, ACE inhibitors, some calcium antagonists) although there is no proof as yet of the benefits of this intervention (which could suppress the adaptation to the increased wall stress of the left ventricle); malignant hypertension and its cardiovascular complications have almost disappeared with modern antihypertensive therapy. Cardiac failure can be effectively prevented and cured when exclusively related to hypertension. When diastolic pressures are lowered by 8-10 mmHg cerebrovascular risk is reduced by a half and coronary risk by a quarter. Cardiovascular mortality related to hypertension is thus reduced by 20% and total mortality is thereby significantly decreased; the large scale clinical trials which provided these data were performed in the years 1965-1985 with diuretic therapy relayed by (or compared with) betablockers from 1980 onwards. These two families remain the drugs of reference in the prevention and treatment of the cardiovascular complications of hypertension. Personalized description of antihypertensive therapy should take into account the degree of risk and previous cardiovascular complications of the hypertensive patient: betablockers eventually associated with calcium antagonists are to be preferred in cases of hypertension with coronary artery disease and/or arrhythmias, severe hypertension and hypertension complicated by cardiac failure are good indications for ACE inhibitors without prejudicing other therapeutic options necessary in certain contexts, in particular aspirin therapy in patients with previous transient ischemic cerebral attacks.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1991 Sep
PMID:[Treatment of hypertension and cardiovascular complications]. 168 21

A sensitive enzyme immunoassay was developed for human angiotensin converting enzyme. Monoclonal antibodies specific for two unique converting enzyme epitopes were utilized to develop a two-site sandwich enzyme immunoassay. Alkaline phosphatase conjugated to the detecting antibody hydrolyzes nicotinamide adenine dinucleotide phosphate (NADP) to NAD. Subsequently, NAD is cycled between its reduced and oxidized forms by an alcohol dehydrogenase/diaphorase catalyzed redox cycle. Each cycle converts iodonitrotetrazolium violet to a highly colored formazan which is quantitated. With this assay, as little as 94 pg/ml of native converting enzyme is detectable without interference from either therapeutic or endogenous converting enzyme inhibitors.
J Immunol Methods 1990 Sep 14
PMID:A sensitive two-site sandwich enzyme immunoassay for human angiotensin converting enzyme utilizing monoclonal antibodies. 169 77

A combination of oral flecainide and mexiletine was given to 11 patients in whom monotherapy with one of these drugs was ineffective for the suppression of inducible ventricular tachycardia or fibrillation. In eight of 11 studies, combination therapy prevented inducibility of a sustained ventricular tachycardia or resulted in induction of only nonsustained tachycardia (P = 0.0003, when compared to monotherapy). In one patient, a slow ventricular tachycardia was induced. During exercise testing ventricular tachycardia occurred in two of these nine patients, and ventricular fibrillation in another patient. Seven patients received combination on the long term, for a mean of 18 months. One patient had recurrences of ventricular tachycardia which was well tolerated. Another patient had a recurrent episode of ventricular fibrillation, but was successfully resuscitated. Severe congestive heart failure occurred in two patients. ACE inhibitors were given to them and to another four patients. No other important unwanted effects occurred. The combination of mexiletine and flecainide is very effective in suppressing inducible sustained ventricular tachycardia. The efficacy of this combination to prevent recurrences of ventricular tachyarrhythmias is acceptable. Exercise testing is of importance to unmask proarrhythmic effects before discharge from hospital.
Pacing Clin Electrophysiol 1990 Sep
PMID:Combination of flecainide and mexiletine for the treatment of ventricular tachyarrhythmias. 170 Mar 88

The influence of angiotensin converting enzyme inhibition on the development of left ventricular (LV) hypertrophy due to stenosis of the aortic arch was studied in female Sprague-Dawley rats. The aortic arch was banded to an outer diameter of 1.0 mm. After 14 days, LV and right ventricular functional parameters and transstenotic pressure gradient were measured in anesthetized rats. In addition, regional heart weights were determined, and myocytes of three different heart regions were isolated and subjected to morphometric analysis. To inhibit the angiotensin converting enzyme, ramipril was administered orally by gavage in a single daily dose of 1 mg/kg. Rats with aortic stenosis showed a marked increase in LV systolic pressure, mean prestenotic aortic pressure, and LV stroke work compared with sham-operated rats and demonstrated a systolic transstenotic pressure gradient of 82 mm Hg. This increase in LV hemodynamic load was paralleled by the development of LV hypertrophy as determined by a 37% increase in LV weight and by a 20% increase in cell volume of isolated LV myocytes. Concomitant ramipril treatment did not significantly affect LV functional parameters. The transstenotic pressure gradient was the same as in untreated rats with aortic stenosis. Likewise, the weight gain of the LV as well as the development of cellular hypertrophy of the LV were not influenced. Thus, in this model, angiotensin converting enzyme inhibition did not reduce the development of LV hypertrophy independent of the hemodynamic load.
Circ Res 1991 Sep
PMID:Effect of angiotensin converting enzyme inhibition on pressure-induced left ventricular hypertrophy in rats. 171 99


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