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 problem of sudden cardiac death (SCD) in the aged impends on 14% of the adult population in the Slovak Republic and it often involves people who are still effectively active. It is now generally known that a person ill with his heart is never too old to benefit from the stratification of his/her cardiovascular risk. In clinical practice it is possible to suggest to use the combination of non-invasive methods as the first step in basic stratification of risk in the aged (Holter ECG monitoring, echocardiographically assessed ejection fraction of the left ventricle, ergometric test). Regarding the prevention of SCD it is necessary to teach the patients at risk to distinguish the symptoms of the impending collapse/SCD. After myocardial infarction, also in the aged, the therapy by acetylosalicylic acid, Beta-blockers and ACE inhibitors is indicated. There are fewer contraindications to this therapy than it has been presented until now. Antiarrhythmic drugs class I are not to be used. Also in the aged, regarding the prevention of tachycardiac SCD, the most prospective antiarrhythmic drugs are amiodaron and sotalol. The attention should be paid also to other factors in coincidence with sudden cardiac death that can be influenced by therapy (consequential antiischaemic therapy, homeostasis of the internal environment, early cardiostimulatory therapy of bradycardiac disturbances of rhythm, optimal timing of surgical therapy of valvular defects if indicated, prevention of pulmonary embolism, etc.). In the aged it is necessary to create a wider space in the field of invasive cardiological therapy. In general it is possible to state that the knowledge on etiopathogenetic stratification and specific characteristics of prevention and therapy of SCD in the aged are limited. This fact only emphasizes the inevitability to concentrate on the research in this area.
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PMID:[Sudden cardiac death in the aged]. 947 34

This work studies damage to rat liver mitochondrial protein, lipid, and DNA caused by electronically excited states generated by cytochrome c-catalyzed diphenylacetaldehyde enol oxidation to triplet benzophenone. The extension of lipid peroxidation was estimated by production of thiobarbituric acid-reactive substances and by formation of Schiff bases with membrane proteins, evaluated by SDS-polyacrylamide gel electrophoresis. Concomitant with DPAA-driven mitochondrial permeabilization, extensive mtDNA fragmentation occurred and DNA adducts with aldehydes-products of fatty acid oxidation-were observed. The degree of lipid peroxidation and mtDNA alterations were significantly decreased by butylated hydroxytoluene, a potent peroxidation chain breaker. The lipid peroxidation process was also partially inhibited by the bioflavonoid rutin and urate totally prevented the mitochondrial transmembrane potential collapse. In all cases, the mitochondrial damage was dependent on the presence of phosphate ions, a putative bifunctional catalyst of carbonyl enolization. These data are consistent with the notion that triplet ketones may act like alkoxyl radicals as deleterious reactive oxygen species on biologic structures. Involvement of singlet dioxygen formed by triplet-triplet energy transfer from benzophenone in the model reaction with DPAA/cytochrome c in the presence of DCP liposomes was suggested by quenching of the accompanying chemiluminescence upon addition of histidine and lycopene.
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PMID:Diphenylacetaldehyde-generated excited states promote damage to isolated rat liver mitochondrial DNA, phospholipids, and proteins. 1051 78

We report a case whose renal failure was due to malignant hypertension and in whom steroid facilitated the recovery of renal function. The patient, a 41-year-old man, was admitted to our hospital because of malaise and macrohematuria. On admission, his blood pressure was 270/160 mmHg. The plasma renin activity (PRA) and aldosterone were markedly elevated. Chest X-ray, echo cardiography and electrocardiogram revealed marked hypertrophy. Hypertensive retinopathy and arteriosclerotic change were noted on ophthalmoscopy. Because of renal dysfunction (blood urea nitrogen 45.6 mg/dl, serum creatinine 4.9 mg/dl with massive proteinuria and increased FENa, renal biopsy was performed on the 8th clinical day. The specimens showed slight proliferation of mesangial cells with mesangiolysis and interstitial cell infiltration, in addition to marked arteriosclerosis and partial collapse of the glomerular tuft. After the administration of a Ca antagonist and angiotensin converting enzyme inhibitor (ACE-I), his mean blood pressure decreased to 100-130 mmHg, and urinary protein decreased as well. Nevertheless, renal dysfunction remained unchanged during the following 3 weeks. Thus, prednisolone (PSL, 30 mg/day) was administered on the 22nd clinical day and renal function improved thereafter without a significant change in blood pressure. The improved renal function was maintained after PSL tapered off on the 184th clinical day. It is suggested that PSL might be the therapy of choice in malignant hypertension, when the renal function has not been improved by anti-hypertensive treatment alone.
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PMID:[A case of malignant hypertension in whom steroid improved renal function]. 1065 31

Autonomic control of blood pressure appears to decline with age giving rise to an increased risk of orthostatic hypotension and major hypotensive reactions to antihypertensive drugs. In the past few years, many workers have assessed autonomic function in the elderly and sometimes found controversial results. Baroreflex sensitivity, as measured by the steepness of the heart rate/mean pressure curve, decreases with age. However, this phenomenon does not correlate well with orthostatic impairment. Sympathetic dysfunction might be more responsible for syncopal symptoms in the elderly, a finding supported by the fact that elderly with orthostatic symptoms never collapse within a few seconds, but do so after 1 or more minutes of standing. However, the results of sympathetic function testing in the elderly indicate that sympathetic function in most elderly is not impaired and that sympathetic activity, as measured by circulating levels of catecholamines, is usually increased rather than decreased. In various populations with increased sympathetic activity, but not in the elderly, beta-adrenoceptor antagonists (beta-blockers) have been demonstrated to cause pressor effects, presumably due to alpha-adrenoceptor-mediated vasoconstriction unopposed by beta-receptor-mediated vasodilation. In the past year, large studies have been completed indicating that the same is true for the elderly, and that the depressor effect on pulse pressure upon standing in this category of patients can be offset and turned into a pressor effect by long-term beta-blocker treatment. This phenomenon could not be demonstrated with non-beta-blocker antihypertensive drugs, including ACE inhibitors, calcium channel antagonists, diuretics and angiotensin II receptor antagonists. In elderly patients beta-blockers may, therefore, be the most appropriate antihypertensive agents as they protect the elderly from orthostatic impairment.
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PMID:Age-related decline in autonomic control of blood pressure: implications for the pharmacological management of hypertension in the elderly. 1269 92

Collapsing glomerulopathy is a morphologic variant of focal segmental glomerulosclerosis (FSGS) characterized by segmental and global collapse of the glomerular capillaries, marked hypertrophy and hyperplasia of podocytes, and severe tubulointerstitial disease. The cause of this disorder is unknown, but nearly identical pathologic findings are present in idiopathic collapsing glomerulopathy and human immunodeficiency virus (HIV)-associated nephropathy, and collapsing glomerulopathy has been associated with parvovirus B19 infection and treatment with pamidronate. The pathogenesis of collapsing glomerulopathy involves visceral epithelial cell injury leading to cell cycle dysregulation and a proliferative phenotype. Clinically, collapsing glomerulopathy is characterized by black racial predominance, a high incidence of nephrotic syndrome, and rapidly progressive renal failure. Collapsing glomerulopathy also may recur after renal transplantation or present de novo, often leading to loss of the allograft. The optimal treatment for collapsing glomerulopathy is unknown. Treatments may include steroids or cyclosporine in addition to aggressive blood pressure control, angiotensin converting enzyme inhibitors and/or angiotensin II receptor blockers, and lipid lowering agents. The role of other immunosuppressive agents such as mycophenolate mofetil in the treatment of collapsing FSGS remains to be defined. Prospective clinical trials are needed to define optimal therapy of this aggressive form of FSGS.
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PMID:Collapsing glomerulopathy. 1270 81

Unilateral ureteral obstruction (UUO) and hyperoxaluria (HOX) can lead to end-stage renal disease with tubulointerstitial fibrosis. We investigated the effects of enalapril (E), an ACE-inhibitor, on rat kidneys with either UUO or HOX. Sham-operated, UUO, HOX, UUO+HOX, UUO+E and HOX+E rats were killed 14 days after UUO and/or HOX was initiated. Rat kidney sections were histologically scored for tissue damage and monocyte/macrophage infiltration was demonstrated with ED1 antibody and measured by computer image analysis software. Serious glomerular and tubulointerstitial damage was found for UUO and HOX, consisting of glomerular basement membrane thickening, tubular dilatation/collapse, tubular basement membrane thickening and the infiltration of mononuclear leucocytes (mainly macrophages). For HOX, calcium oxalate crystals were visible. Neither the scored histological parameters nor monocyte/macrophage infiltration was significantly decreased when E-treated were compared with untreated groups. We conclude that E did not ameliorate the parameters scored in either UUO or HOX. This being contrary to findings by other research groups, we hypothesize that E may be effective only in short-term UUO/HOX, with transforming growth factor, TGF-beta1, formation becoming partly independent of Ang II in late-stage UUO/HOX, or other fibrogenic cytokines than TGF-beta1 becoming predominant.
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PMID:Is enalapril adequate for the prevention of renal tissue damage caused by unilateral ureteral obstruction and/or hyperoxaluria? 1271 49

We tested the effect of ACE inhibition on the survival of bovine retinal (REC) and choroidal (CEC) endothelial cells (EC) in culture. The ACE inhibitor captopril delayed the apoptotic tube collapse of REC on Matrigel for >15 days. Captopril treatment of confluent monolayers (2-8 weeks) followed by slow starvation (2-4 weeks) increased EC viability by approximately 200%. Two-week captopril exposures were sufficient to confer maximal protection. Only vehicle-treated EC demonstrated apoptotic features such as membrane blebbing and DNA laddering. By RT-PCR, the starvation marker p202 was upregulated only in starved cells. In REC, captopril upregulated the pro-survival proteins mortalin-2, uPA, and uPAR while downregulating the anti-growth sprouty-4 and tPA. In CEC, captopril also upregulated tPA and its inhibitor PAI-1. Amiloride (uPA inhibitor) blocked the captopril-induced increase in EC survival, secondary sprouting, and invasion in Matrigel. The pro-survival effects of captopril involve the reprogramming of genes involved in cell survival and immortalization.
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PMID:ACE inhibition actively promotes cell survival by altering gene expression. 1455 46

Angioedema can be a symptom of anaphylaxis; it may be more hazardous that the circulatory collapse in otherwise healthy patients. Angioedema can be part of IgE- and histamine-mediated allergic reactions or part of NSAID-induced hypersensitivity with disturbances in arachidonic acid metabolism. If angioedema occurs without urticaria or other symptoms of anaphylaxis, it is usually mediated by increased bradykinin synthesis (HANE, EANE) or reduced metabolism (ACE inhibitors). These observations have led to new therapeutic approaches in HANE. Icatibant is a bradykinin-receptor-2 antagonist and blocks bradykinin-induced angioedema in HANE. How applicable this will be to ACE-inhibitor angioedema remains to be seen.
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PMID:[Angioedema]. 1800 29

In this study, we have attempted to reveal the physical or mechanistic features of the sonochemical degradation of 2,4-dichlorophenol (2,4-DCP). The principal physical phenomenon underlying sonochemical effects is radial motion of cavitation bubbles and production of radicals from transient collapse of these bubbles. We reveal some important physical facets of sonochemical degradation of 2,4-DCP by adopting dual approach of coupling experimental results with simulations of radial motion of cavitation bubble. First, the location of the degradation is predominantly the interfacial region between bubble and bulk medium, and secondly, the extent of degradation is controlled by conservation--and not the production--of oxidizing radicals that affects the probability of radical-pollutant interaction.
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PMID:Physical insight into the sonochemical degradation of 2,4-dichlorophenol. 2127 46

Circulating angiotensin-II protects the circulation against sudden falls in blood pressure and is generated by the enzymatic action of angiotensin converting enzyme (ACE) on angiotensin-I. The ACE genes have 2 allelic forms, "I" and "D." The "D" genotype has both highest angiotensin-II generation and serum ACE levels compared to "I". 120 patients with IgE-anaphylaxis, 119 healthy controls, and 49 atopics had serum ACE levels, ACE genotype, and renin levels determined. Plasma renin levels were identical for all groups. Serum ACE levels and genotypes were similar for healthy controls (HC) and atopics, but lower in anaphylaxis (P = 0.012), with ACE genotypes also showing increased "I" genes (P = 0.009). This effect was more pronounced in subjects manifesting airway angioedema and cardiovascular collapse (AACVS) than mild cutaneous and respiratory (CRA) symptoms. AACVS was significantly associated with the presence of "I" genes. For "ID" genotype OR is 5.6, 95% CI 1.8 to 17.4, and for "II" genotype OR is 44, 95% CI 5 to 1891 within the anaphylaxis group = 0.001. The results show a difference in the genotype frequency between control and anaphylaxis, suggesting a role for the renin angiotensin system in anaphylaxis manifesting with airway angioedema and cardiovascular collapse.
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PMID:IgE-Mediated Anaphylaxis to Foods, Venom, and Drugs: Influence of Serum Angiotensin Converting Enzyme Levels and Genotype. 2331 49


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