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)

Left ventricular dysfunction is asymptomatic or paucisymptomatic for a long time. It would be beneficial if progression to the symptomatic stages could be prevented. This is only possible when the abnormal conditions of cardiac load or perfusion which cause the myocardial disease, can be corrected. The treatment of hypertension or valvular disease is an example of this approach. Another approach is to reduce the perverse effects of the neurohormonal adaptations to cardiac failure. The treatment of chronic myocardial infarction by angiotensin converting enzyme inhibitors is an example of this approach.
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PMID:[Can ventricular dysfunction be prevented or delayed in course?]. 214 70

Hypertension and cardiomyopathy are prominent findings in humans and rats harboring pheochromocytomas, tumors that can secrete enormous quantities of catecholamines. We have previously found that alpha- and beta-adrenergic receptor antagonists may ameliorate the hypertension and cardiomyopathy found in New England Deaconess Hospital rats implanted with pheochromocytoma. The present studies were designed to determine the possible action of the angiotensin converting enzyme inhibitor captopril on these changes in rats harboring pheochromocytomas. Rats were implanted with transplantable pheochromocytomas and treated with captopril dissolved in the drinking water (1 mg/ml) for 4-6 weeks. Systolic blood pressure was monitored by using the tail-cuff technique. In the rats with pheochromocytoma, blood pressure progressively increased to 184 +/- 3 mm Hg after the tumor was implanted. However, in rats with pheochromocytoma treated with captopril in the drinking water before the development of hypertension, blood pressure did not increase (137 +/- 3 mm Hg). In rats with pheochromocytoma with established hypertension, captopril normalized the systolic blood pressure. Plasma norepinephrine was markedly elevated to a similar extent in both groups compared with unimplanted control rats. Plasma renin activities were slightly lower in rats with pheochromocytoma compared with unimplanted control rats. Treatment with captopril of rats with pheochromocytoma did not modify contraction of isolated rings of thoracic aorta exposed in vitro to either phenylephrine or angiotensin II. Treatment with captopril markedly attenuated the cardiomyopathy induced by pheochromocytoma. These results demonstrate that captopril prevents the development of hypertension despite markedly elevated concentrations of catecholamines. In addition, captopril attenuates catecholamine-induced cardiomyopathy in pheochromocytoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril improves hypertension and cardiomyopathy in rats with pheochromocytoma. 215 6

We examined the hypothesis that the positive inotropic effect of angiotensin I (Ang I) may be retained in the presence of angiotensin converting enzyme inhibitors so that it may have a direct beneficial effect on the heart. Accordingly, isolated perfused hearts (Langendorff preparation) of 300-day-old cardiomyopathic hamsters (a model of spontaneous cardiomyopathy) and age-matched normal hamsters (controls) were infused with Ang I in the presence of captopril; propranolol was added to the perfusing medium to block catecholamine-mediated effects of angiotensins on the heart. Left ventricular developed pressure and the rate of increase in left ventricular developed pressure increased significantly (p less than 0.001) in both the cardiomyopathic and the normal hamster heart despite concomitant reduction in myocardial flow rate favoring a direct inotropic effect of Ang I in both normal and myopathic hearts; these changes were significantly higher by almost threefold in the cardiomyopathic than in the normal hamsters (p less than 0.01) and were blocked by the angiotensin II (Ang II) antagonist [Sar1,Thr8]Ang II. Comparing dose-left ventricular contractility response curves for Ang I and Ang II, ED50 for responses was identical in both normal and myopathic hearts, whereas peak responses to Ang II were double those to Ang I in normal hearts but were almost identical in the myopathic hearts. Binding of [125I]Ang II in six cardiomyopathic and four normal hamster hearts was of high affinity, but there was no evidence for Ang I-saturable high-affinity binding sites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensins and the failing heart. Enhanced positive inotropic response to angiotensin I in cardiomyopathic hamster heart in the presence of captopril. 218 May 88

Recent evidence suggests that the most common form of idiopathic cardiomyopathy in our altitudes, the dilated cardiomyopathy (DCM), is a post-infectious autoimmune disease which is triggered by virus infections. In animal experiments, the development of the coxsackie virus B3 myocarditis to a congestive cardiac insufficiency resembling the clinical picture of DCM was demonstrated. In mice, species-dependent varying disease courses could be observed, which point to a genetically different behaviour of the animals' immunological reactions, either humoral or T-cell mediated immune reactions being responsible. In comparison with non-DCM patients, patients with DCM and chronic myocarditis exhibit significantly higher coxsackie virus antibody titres. Obviously, also a differently long viral persistency in the cardiac muscle plays a role, as enterovirus-specific RNA was detected in myocardial biopsies from patients with DCM. Along with myocardial fibroses, endomyocardial biopsies in DCM frequently reveal mononuclear cellular infiltrates, which, however, only in 20-25% of the cases may be regarded as chronic persisting myocarditis. The clinical and paraclinical findings in DCM and in the so-called latent cardiomyopathy are presented. In congestive heart failure, the best therapeutic results are achieved by the ACE inhibitors, along with vasodilator agents, digitalis glycosides and diuretics. Ultima ratio is the orthotopic heart transplantation, as it is only this intervention that will be able to improve the primarily bad prognosis decisively. Whether the treatment with immunosuppressive drugs exerts an influence upon the prognosis, has thus far remained an open question.
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PMID:[Dilated cardiomyopathy--heart muscle disease of unknown origin or an autoimmune disease? New aspects of etiology, pathogenesis and clinical practice]. 268 30

This report describes the case of a 70-year-old female suffering from diabetes mellitus and dilatative cardiomyopathy with congestive heart failure. It is likely that alveolar-capillary membrane damage occurred apart from cardiac involvement. Diffuse interstitial pulmonary fibrosis subsequently occurred with consequent acute progressive respiratory failure and death. The cause of the damage to the alveolar-capillary membranes is still unknown and we thought that long-term administration of captopril might have contributed to the damage itself, since like all ACE-inhibitors, captopril is able to bring about tissular storage of both bradykinin and prostaglandins and therefore alter the pulmonary reactivity to phlogistic stimuli.
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PMID:[Acute progressive respiratory insufficiency caused by diffuse interstitial pulmonary disease in a diabetic patient with dilated myocardiopathy]. 270 34

As first reported by our group in 1975, severe heart failure due to idiopathic dilated cardiomyopathy could be improved in patients receiving beta-blocker therapy starting at a very low dose and followed by a stepwise increase. Since then, these results have been confirmed by our own group and by others, and similar results were also obtained in patients with other forms of cardiomyopathy, including ischaemic cardiomyopathy. In 13 separate studies involving a total of 651 patients with idiopathic dilated cardiomyopathy, beta-blockade for 2 to 19 months (in addition to conventional treatment of heart failure, including angiotensin converting enzyme inhibitor therapy), significantly improved cardiac function. These studies were performed using metoprolol, bucindolol, labetalol and practolol. Eight studies investigated the effects of long term beta-blocker treatment in patients with heart failure and cardiomyopathy due to coronary artery disease, valvular heart disease, diabetes and doxorubicin therapy. A total of 128 patients were treated with metoprolol, carvedilol or bucindolol for periods of 2 to 12 months. All studies reported a significant improvement in cardiac function. Three studies reported results on survival and the need for cardiac transplantation. The first study published by our group reported improved survival in patients with idiopathic dilated cardiomyopathy treated with metoprolol plus digitalis and diuretics compared with a matched control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of beta-blockers in the treatment of cardiomyopathy and ischaemic heart failure. 752 60

The purpose of this study was to determine tissue angiotensin I-converting enzyme (ACE) activity in aging hamsters with and without cardiomyopathy, and the factors that regulate its activity in vitro. We found that ACE activity was significantly increased in the heart and significantly decreased in the lung of aging hamsters with hereditary cardiomyopathy in comparison to age/genetically-matched controls (P < 0.05). Kidney and cheek pouch ACE activity was similar in both groups. Lisinopril inhibition curves of tissue ACE activity were similar in aging hamsters with and without cardiomyopathy. In both groups, tissue ACE activity was dependent on chloride anion concentration in the assay buffer. Substituting citrate for chloride abrogated, in part, this response. We conclude that cardiomyopathy is associated with significant changes in cardiac and lung ACE activity in aging hamsters in comparison to age/genetically-matched controls. However, regulation of tissue ACE activity in vitro is similar in both groups.
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PMID:Tissue angiotensin I-converting enzyme activity in aging hamsters with and without cardiomyopathy. 759 97

The effects of an angiotensin converting enzyme (ACE) inhibitor on the intrinsic contractility of the myocardium in cardiac failure have not been studied intensively. The authors studied inotropism, lusitropism and economy of contraction in vitro on left ventricular papillary muscle preparations of cardiomyopathic Syrian hamsters (CSH) treated preventively with perindropil, i.e. before overt signs of cardiac failure. The CSH of the dilated Bio 53.58 strain aged 1 month were treated with perindropil 1 mg/Kg/day for 5 months (PE, N = 11) or with placebo (PL, N = 11) and control hamsters of the F1B strain received placebo (C, N = 7). Compared with C, PL had a significant reduction of the maximal velocity of contraction Vmax (p < 0.01) and of total isometric tension (TF/mm2), p < 0.05, and a reduction of the G curve of the hyperbolic Hill Force-Velocity relationship (p < 0.01). The G value is usually greater in models with improved economy of contraction. When compared with PL, PE showed a 68% inhibition of the plasma activity of ACE, a better Vmax (p < 0.05) but an unchanged TF/mm2. The G value was less depressed than that of C (p < 0.05). The velocity of isotonic relaxation (maxVL) and the negative peak of the derivative of the isometric force (-dF/dt max) were significantly lower in the PL than in the C group but these lusitropic abnormalities remained coordinated with those of the contraction phase, indicating the absence of an intrinsic effect on relaxation in cardiomyopathy. Perindopril prevented the reduction of maxVL but not that of -dF/dt max.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Protective effects of perindopril in an experimental model of cardiomyopathy]. 821 90

The term heart failure has become a label for more than one clinical entity. For many years heart failure has been used to denote patients with various heart diseases who have begun to suffer from fluid retention, pulmonary venous hypertension, or systemic venous hypertension, either alone or in combination. More recently, the term heart failure has been applied to the combination of effort intolerance and reduced left ventricular contractility due to ischemic heart disease or other myocardial disease. Comparison of the results of epidemiological studies and therapeutic trials is complicated by variation in the composition of the patient populations selected for study. Drug treatment of heart failure remains fairly empirical. Distinction should be made between immediate or prognostic benefits related to the etiological diagnosis, and benefits related specifically to prevention and relief of, for example, fluid retention, rhythm disturbances, or ventricular hypertrophy. The response of individual patients to several forms of drug treatment, including digoxin, ACE inhibitors, and beta-blockade, is unpredictable. Prospective identification of patients liable to respond well to these drugs is not yet possible, but would greatly assist the choice of treatment. At present, trial of therapy is required in each patient to establish benefit and to avoid long-term treatment of nonresponders.
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PMID:The management of heart failure: a matter of definition? 824 Oct 9

The haemodynamic effects of the sulfhydryl-containing angiotensin converting enzyme inhibitor, zofenopril, were studied in patients in New York Heart Association functional class II and III. Twenty-one clinically stable patients with coronary artery disease or cardiomyopathy completed a randomized double-blind treatment period of 2 months with either 15 mg zofenopril once daily or placebo. Regular therapy with digoxin and diuretic drugs was continued. Left ventricular volumes were measured by radionuclide angiography at rest and during submaximal bicycle exercise. Zofenopril significantly increased mean stroke volume at rest from 59 to 67 ml (48 vs 48 ml in the control group, 95% confidence interval of the difference 1 to 16 ml) and left ventricular ejection fraction at rest from 39 to 43% (30 vs 30% in the control group, 95% confidence interval of the difference 1 to 8%). No significant changes occurred in heart rate, cardiac output, and blood pressure at rest, and zofenopril did not result in haemodynamic alterations during exercise. Thus, 15 mg of the sulfhydryl-containing angiotensin converting enzyme inhibitor, zofenopril, administered once daily to patients with moderate heart failure increases left ventricular function at rest, but not during exercise.
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PMID:Angiotensin converting enzyme inhibition at rest and during exercise in congestive heart failure. 850 63


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