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)

Experiments with rabbit platelets in vitro revealed differences in the effect of the aggregation inducers (ADP and thrombin) and the aggregation inhibitor cyclic AMP on the activity of the enzymes of pentosephosphate pathway of glucose oxidation. ADP and thrombin decrease significantly the activity of glucoso-6-phosphate dehydrogenase (G-6-PDH) and riboso-5-phosphate-metabolizing enzymes (R-5-PME) in platelets during aggregation, whereas cyclic AMP produces no appreciable effect on the G-6-PDH activity, but increases significantly the R-5-PME activity. ADP decreases and cyclic AMP raises substantially the activity of R-5-PME. The differences were also revealed in the effects produced by cyclic AMP and cyclic GMP on the enzymes of pentosephosphate pathway of glucose oxidation. Unlike cyclic AMP, cyclic GMP decreased significantly the activity of G-6-PDH. The activity of R-5-PME and cyclic GMP transketolase was more pronounced than that of cyclic AMP. Like cyclic AMP, cyclic GMP differs from ADP and thrombin in the action produced on the enzymes of pentosephosphate pathway of glucose oxidation.
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PMID:[Effect of aggregation inducers and inhibitors on the pentosephosphate pathway enzymes of glucose conversion in the thrombocytes]. 22 Dec 44

Whereas mesangial and epithelial cells from glomeruli are commonly grown in vitro, there has been a failure to isolate and propagate human glomerular capillary endothelial cells. This study defines the conditions for the reproducible isolation and growth of homogeneous monolayers of primate (baboon and human) glomerular capillary endothelial cells. Using selective media and growth factors, the following criteria were identified to optimize the isolation and proliferation of glomerular endothelial cells: (1) collagenase treatment of isolated glomeruli; (2) requirement for 20% serum, endothelial cell growth factor and heparin; (3) requirement of fibronectin as surface matrix; and (4) isolation from donors less than 60 years old, as premature senescence was directly proportional to the age of the human kidney donor. Under these conditions, primary cultures with an endothelial cell composition greater than 70% were reproducibly obtained. Homogeneous endothelial monolayers were developed from 20 of 23 human kidneys, and maintained for 5 to 10 passages, depending on the age of the kidney donor. Purification to homogeneity was achieved by patch cloning or by fluorescence-activated cell sorting. Glomerular capillary endothelial cells exhibited a cobblestone morphology at confluence, expressed factor VIII-related antigen, angiotensin converting enzyme activity, and endocytosed acetylated low-density lipoproteins. Electron microscopy revealed the presence of intracellular Weibel-Palade bodies and caveolae and microvillous projections on the luminal surface. Glomerular cells also stained positive for Ulex europaeus, a lectin characteristic of human endothelial cells. In addition, preliminary results indicate that human glomerular endothelial cells increase intracellular cyGMP in response to alpha-human 5 to 28 atrial natriuretic peptide and intracellular free calcium in response to thrombin.
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PMID:Culture of endothelial cells from baboon and human glomeruli. 150 7

Paraquat is a herbicide known to cause pulmonary edema in its acute toxic phase. Many investigators showed that paraquat induces morphological changes of alveolar epithelial cells even in its early phase. Controversy still exists, however, as to whether pulmonary vascular endothelial cells are also morphologically vulnerable to paraquat. To test the direct toxicity and metabolic changes of pulmonary vascular endothelial cells after paraquat addition, porcine pulmonary artery endothelial cells (PPAEC) were cultured. Thrombin- or bradykinin-stimulated PGI2 production was enhanced significantly, and the angiotensin converting enzyme (ACE) activity of cell lysate of PPAEC was significantly suppressed after a 24-hour incubation with 10(-4) M of paraquat. No further thrombin-induced enhancement of PGI2 production was noted after a 48-hour incubation. The alterations in arachidonic acid metabolism and ACE activity mentioned above did not result from cytotoxicity of paraquat because LDH release into culture medium was not increased during 72 hours of incubation with paraquat. Longer incubation more than 48 hours, in turn, induces obvious toxic effects on PPAEC.
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PMID:[Arachidonic acid metabolism and angiotensin converting enzyme activity by cultured porcine pulmonary artery endothelial cells are affected with paraquat]. 166 45

Induction of intravascular coagulation and inhibition of fibrinolysis by injection of thrombin and tranexamic acid (AMCA) in the rat gives rise to pulmonary and renal insufficiency resembling that occurring after trauma or sepsis in man. Injection of Captopril (1 mg/kg), an inhibitor of angiotensin converting enzyme (ACE), reduced both pulmonary and renal insufficiency in this rat model. The lung weights were lower and PaO2 was improved in rats given this enzyme-blocking agent. The contents of albumin in the lungs were not changed, indicating that Captopril did not influence the extravasation of protein. Renal damage as reflected by an increase in serum urea and in kidney weight was prevented by Captopril. The amount of fibrin in the kidneys was also considerably lower than in animals which received thrombin and AMCA alone. It is suggested that the effects of Captopril on the lungs may be attributable to a vasodilatory effect due to a reduction in the circulating level of Angiotension II and an increase in prostacyclin (secondary to an increase in bradykinin). Captopril may, by the same mechanism, reduce the increase in glomerular filtration that is known to occur after an injection of thrombin, thereby diminishing the aggregation of fibrin monomers in the glomeruli, with the result that less fibrin will be deposited and thus less kidney damage will be produced.
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PMID:Effects of an inhibitor of angiotensin converting enzyme (Captopril) on pulmonary and renal insufficiency due to intravascular coagulation in the rat. 267 Jul 94

A versatile, convenient assay for vertebrate collagenases has been developed using the fluorescent peptide substrate dansyl-Pro-Gln-Gly-Ile-Ala-Gly-D-Arg. This sequence resembles that of collagen at the site of cleavage but includes modifications designed to eliminate nonspecific hydrolysis by contaminating peptidases. Both human skin fibroblast and bovine corneal cell collagenases cleave the substrate specifically at the Gly-Ile bond. Plasmin, thrombin, trypsin, alpha-chymotrypsin, carboxypeptidase B, and bacterial collagenase do not cleave the substrate. Elastase and angiotensin converting enzyme display 20- and 400-fold less activity than the vertebrate collagenases, respectively, and cleave the peptide at different positions. The assay is performed by incubating a 5- to 25-microliters aliquot of trypsin-activated sample with an equal volume of 2 mM substrate overnight at 33 degrees C and pH 7.5. Thin-layer chromatography then separates the fluorescent product from the substrate in less than 20 min and allows the detection of subnanogram levels of collagenase. The assay is applicable to the screening of large numbers of samples under different conditions of pH and ionic strength and is readily adaptable for use in a variety of collagenase-dependent systems, such as assays for collagenase activating and/or inducing factors.
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PMID:A convenient fluorescent assay for vertebrate collagenases. 301 20

A disturbing interaction of PAN membranes and the bradykinin generation system particularly in the presence of angiotensin converting enzyme inhibitors has been described. A modified new membrane, SPAN (special PAN), was produced by varying the polymer components in type and composition, in particular by a reduction in Na-Methallylsulfonate. Although the SPAN membrane successfully averted the bradykinin generating ability of PAN, it was important to determine whether such a modification did not lead to a loss of the satisfactory biocompatibility profile characteristic of the parent membrane. For this purpose, we conducted the present clinical study in nine patients comparing 3 membranes; (i) a polysulphone membrane (F60S); (ii) PAN; and (iii) SPAN, to examine the clinical biocompatibility profile and performance of the new membrane. A small increase in C5a with F60S and SPAN was found which is in the range expected for highly biocompatible synthetic membranes. The three dialysers had a similar inert profile for terminal complement complex arterial values, and had similar venous values. A minimal nonsignificant decline in white cell count was observed at 15 min for all dialysers, but otherwise WBC counts were unchanged. Platelet counts were unchanged throughout treatment for the three dialysers. Arterial and venous thrombin-anti-thrombin complex values were similar for all three dialysers. F60S and SPAN dialysers had similar urea clearances.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Synthetic modification of PAN membrane: biocompatibility and functional characterization. 749 15

We investigated the potency of various serotypes of lipopolysaccharides (LPS) by examining LPS-induced stimulation of PGI2 production and suppression of ACE activity in cultured human umbilical vein endothelial cells (HUVEC). HUVEC which had been incubated with E. coli 055:B5 and 0111:B4 for 24 h produced more prostacyclin (PGI2) in response to thrombin than HUVEC incubated with E. coli 026:B6. Also, angiotensin converting enzyme activity (ACE) in cell lysates of HUVEC incubated for 24 h with 055:B5 or 0111:B4 was suppressed significantly compared to control HUVEC or HUVEC incubated with 026:B6. From these experimental results, E. coli 055:B5 and 0111:B4 appear to be more potent than 026:B6. It is concluded that this difference in potency among various serotypes of LPS should be taken into account when experiments are designed to examine the effect of LPS on endothelial cell function.
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PMID:Comparison of the potency of various serotypes of E. coli lipopolysaccharides in stimulating PGI2 production and suppressing ACE activity in cultured human umbilical vein endothelial cells. 814 Jan 23

In order to investigate the feasibility of angiotensin converting enzyme inhibitors (ACEIs) in preventing the development of atherosclerosis and restenosis after coronary angioplasty and to study their mechanisms, we measured the platelet cytosolic free Ca2+ concentration ([Ca2+]i) and observed the effects of captopril on platelet [Ca2+]i in rabbits and also observed the inhibitive action on fibroblast proliferation in culture. The results showed that resting platelet [Ca2+]i,ADP- or thrombin-stimulated platelet elevation amplitude after administration of captopril (12.5 mg, twice daily) for 15 days were significantly reduced in comparison with those before administration. And captopril also significantly inhibited fibroblast proliferation or reduced 3H-thymidine (3H-TdR) incorporation in culture in a dose-dependent manner. These findings suggest that ACEIs are promising drugs to reduce restenosis incidence after coronary angioplasty and to prevent atherosclerosis as well as provide a new explanation for their effects of suppressing cell proliferation.
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PMID:Effects of captopril on platelet cytosolic free Ca2+ concentrations and on suppression of cell proliferation in culture. 829 69

The herbicide paraquat (PQ) is known to cause acute pulmonary edema at toxic dose and to induce morphologic changes in alveolar epithelial cells, even in the early phase of toxicity. However, whether the pulmonary vascular endothelial cells are specifically vulnerable to PQ is still controversial. To investigate the direct toxic and metabolic effects of PQ on pulmonary vascular endothelial cells, cultured porcine pulmonary artery endothelial cells (PPAEC) were evaluated. A dose of 10(-4) M of PQ inhibited the growth of endothelial cells. The thrombin- and bradykinin-stimulated production of prostacyclin (PGI2) by PPAEC was significantly enhanced, and the angiotensin converting enzyme (ACE) activity of cell lysate of PPAEC was significantly suppressed after incubation for 24 h with 10(-4) M PQ. No further enhancement of PGI2 production in response to thrombin after 48 h of incubation was demonstrated. These alterations in arachidonic acid metabolism and ACE activity did not result from the cytotoxicity of PQ, because the release of lactate dehydrogenase (LDH) into the culture medium increased only after 72 h incubation with PQ. Incubation for more than 48 h induced an obvious toxis effect on PPAEC.
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PMID:PGI2 production and angiotensin converting enzyme activity in cultured porcine pulmonary artery endothelial cells treated with paraquat. 838 64

Endothelial cell damage, which is associated with local thrombin formation and inflammation, can lead to the release of endothelium-synthesized factors into plasma, such as vWFAg, TM, ACE and ET-1. These markers of endothelial damage are increased in some patients with diabetes mellitus, but the differences with normal are often small and not closely correlated with the severity of microvascular disease, as judged from the degree of albuminuria and the severity of retinopathy. Prorenin, which may also be related to abnormal endothelial cell function or endothelial damage, is elevated in many patients with diabetes, both type I and II, and its level is more closely correlated with the severity of microvascular disease. It is already elevated at an early stage. Further studies will reveal whether, in diabetes, an increased plasma prorenin is a reliable predictor of progressive microvascular disease. It is even conceivable that prorenin is not only a marker of diabetic microvascular disease but also has a role in its pathogenesis, via local proteolytic or non-proteolytic prorenin activation.
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PMID:Renin-angiotensin system components and endothelial proteins as markers of diabetic microvascular disease. 851 38


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