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)

To investigate the contribution of a cardiac renin-angiotensin system to cardiac hypertrophy due to volume overload, the effects of losartan, a non-peptide angiotensin (Ang) II type 1 (AT1) receptor antagonist on left ventricular hypertrophy (LVH) was studied. LVH was produced in male Wistar rats by volume overload secondary to aortic insufficiency (AI). Losartan (10 mg/kg/d) was orally administered for 2 weeks after surgery to both AI and sham-operated (control) rats. Two weeks after surgery, aortic pulse pressure and left ventricular (LV) weight were markedly increased in the AI rats as compared with the control group, whereas cardiac angiotensin converting enzyme (ACE) activity remained unchanged. The effects of the chronic administration of losartan an AT1 receptors were verified by the blockade of Ang II pressor response. Losartan treatment produced a significant reduction in LVH in AI rats without affecting the systolic blood pressure. In separate groups of rats, to elucidate the mechanisms of the attenuation of LVH by treatment with losartan, we determined plasma and LV immunoreactive Ang II content and plasma renin activity (PRA). LV Ang II content increased in AI rats, while plasma Ang II content, PRA and II concentration were increased by the treatment. There was a significant positive correlation between LV weight and LV Ang II content. These results suggest that cardiac Ang II, rather than circulating Ang II, plays an important role in the LVH due to volume overload via the AT1 receptor.
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PMID:Effects of losartan, an angiotensin II antagonist, on the development of cardiac hypertrophy due to volume overload. 749 86

This study was performed to assess the effects of one year of ACE inhibition with quinapril on left ventricular performance and morphology in asymptomatic patients with chronic aortic regurgitation. Pre- and afterload reduction is known to have beneficial effects in patients with chronic aortic regurgitation. To date, no controlled study has been reported analyzing long term influence of ACE inhibitor treatment on asymptomatic patients with chronic aortic regurgitation. Twelve asymptomatic patients with isolated moderate to severe chronic aortic regurgitation, no coronary disease on coronary angiography and no previous vasodilator treatment were studied under control conditions and after three and 12 months of quinapril therapy (10-20 mg/day) using echocardiography and simultaneous right heart catheterization and radionuclide ventriculography at rest and during supine bicycle exercise. After one year quinapril therapy regurgitant fraction fell by 17% compared to control before therapy (p = 0.001), left ventricular enddiastolic volume at rest was reduced from 150 +/- 33 to 128 +/- 30 ml/m2 (p = 0.0003) and endsystolic volume decreased from 55 +/- 27 to 44 +/- 28 ml/m2 (p = 0.0005). Left ventricular ejection fraction at rest averaged 0.64 +/- 0.11 at control and increased after one year therapy to 0.67 +/- 0.11 (p = 0.05). With maximum exercise (100 W), ejection fraction failed to rise at control; after one year therapy with quinapril it increased to 0.70 +/- 0.15 (p = 0.019). Moreover, after one year quinapril therapy there was a significant reduction of 35% in left ventricular mass compared to control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of 12 months quinapril therapy in asymptomatic patients with chronic aortic regurgitation. 800 May 84

Amyloidosis results from protein infiltration of the extracellular space of organs and tissues. Several amyloidosis proteins have been identified. Protein AL, (deriving from immunoglobulin light chain), protein AA and prealbumin are the most involved in this disease. When AL amyloidosis involves the heart, the illness is often terminal. Most clinical symptoms are heart failure and arrhythmia or block conduction. This case was characterised by the unusual combination of hypertension and amyloidosis. The diagnosis suggested by the echocardiographic but was confirmed by the damaged organ's biopsy. The present case concerns a young woman, who has hypertension and a pulmonary oedema. The echocardiographic scan showed a septal hypertrophy with a shining and granite-like aspect which is compatible with heart amyloidosis. Systolic and diastolic disorder with mitral and aortic regurgitation were also revealed. The kidney and rectum biopsies confirmed amyloidosis AL of the Kappa dysglobulinemia type, without extraosseous plasmocytoma. The heart and kidney failure symptoms disappeared after treatment with diuretics and ACE inhibitors.
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PMID:[Heart failure and arterial hypertension disclosing amyloidosis]. 929 35

Long-term treatment with ACE-inhibitors improves left ventricular function in patients with aortic regurgitation. But how does this advantage influence capacity? Using echocardiography and spiroergometry, we investigated 13 patients before and after a 3 month treatment with cilazapril (2.5-5 mg/d). Ventricular enddiastolic diameter-index decreased from 3.5 to 3.1 cm/m2 (p = 0.005), left ventricular endsystolic diameter-index from 2.3 to 2.0 cm/m2 (p = 0.005), and wallstress from 174 to 150 dyn/cm2 (p = 0.01). Left ventricular mass was reduced by 14% to 488 g (= 253 g/m2, p < 0.05). The regurgitant jet area decreased from 10.1 to 8.1 cm2 (p < 0.05). Wall thickness, workload, and maximal oxygen intake showed no significant difference during follow-up. These results indicate that left ventricular volumes and muscle mass in patients with aortic regurgitation are positively influenced by long term ACE-inhibition, which preserves exercise capacity.
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PMID:[Follow-up of patients with chronic aortic valve insufficiency with ACE inhibitor therapy]. 949 99

The effect of the angiotensin converting enzyme (ACE) inhibitor, captopril, on proteosynthesis in the aorta, acetylcholine-stimulated aortic relaxation and endothelaemia (circulating endothelial cells) was investigated in rabbits with aortic insufficiency. The animals were studied 28 days after experimental intervention. Cardiac volume overload stimulated proteosynthesis in the aorta as reflected by increased ribonucleic acid (RNA) concentration and [14C] leucine incorporation into proteins of the aorta. Moreover, the number of endothelial cells in the blood was increased. The administration of captopril starting from the second day of the haemodynamic overload, partially prevented the increase both in aortic proteosynthesis and in endothelaemia. Despite these alterations, the relaxing ability of the aorta to acetylcholine was not changed either by the haemodynamic overload or by captopril. We conclude that the increase of proteosynthesis in the aorta and of endothelaemia in the early period of chronic cardiac volume overload in rabbits were partially prevented by chronic captopril treatment. Neither aortic insufficiency nor captopril changed the acetylcholine-induced relaxation of the aorta.
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PMID:Captopril attenuates proteosynthesis in the aorta and decreases endothelaemia in rabbits with aortic insufficiency. 970 92

HLA-DNA typing using PCR-SSOP and PCR-DCP methods was performed in 85 patients with Takayasu arteritis and 492 healthy controls who had been typed for HLA by serological method. Frequencies of HLA-B52 (B*5201) and B39 (B*3901 and B*3902) were significantly increased in the patients. Frequency of HLA-DRB1*1502 was also increased but it was suggested to be a reflection of its linkage disequilibrium with B52. Association of HLA-B52 and B39 with seven clinical manifestations--pulmonary infarction, ischemic heart disease, aortic regurgitation, systemic hypertension, renal artery stenosis, cerebrovascular disease, and visual disturbance--in 132 HLA-typed patients with Takayasu arteritis was studied. In HLA-B52 positive TA patients, aortic regurgitation (vs B52(-)-B39(+), OR=3.8, P<0.05, vs B52(-)-B39(-), OR=5.49, P<0.001), ischemic heart disease (vs B52(-)-B39(+), OR=12.05, P<0.05, vs B52(-)-B39(-), OR=2.85, P<0.05), and pulmonary infarction (vs B52(-)-B39(+), OR=5.74, P<0.03) were found to be significantly prevalent. On the other hand, in HLA-B39 positive TA patients, frequency of renal artery stenosis was significantly increased (vs B52(+)-B39(-), OR=12.14, P<0.001, vs B52(-)-B39(-), OR=5.21, P<0.03). These observations have suggested that HLA-B52 molecule and B39 molecule would contribute to different clinical manifestations by binding different antigenic peptides to cause inflammations. Thus HLA-B molecule may play an important role in pathogenesis or determining clinical manifestations of Takayasu arteritis.
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PMID:Association of clinical manifestations with HLA-B alleles in Takayasu arteritis. 995 11

This review has been focused on the new insights in the pathophysiology of mitral and aortic regurgitation and on the role of ACE-inhibitor therapy in children with chronic volume overload due to left-sided valvular lesions. Recent clinical studies show that these drugs have favorable effects when administered orally in chronic mitral and aortic regurgitation. Interestingly, the beneficial effects of ACE-inhibition regard the basic anatomic, hemodynamic and adaptive pathologic conditions related to volume overload, namely, the regurgitant orifice area and volume and ventricular remodeling. The heart is a plastic structure, constantly being altered in size, shape and composition in response to chronic volume overload. Thus, modulation of cardiac plasticity by ACE-inhibition raises the possibility of using new therapeutic strategies specifically designed to prevent and/or antagonize the mechanical disadvantages secondary to volume overload-induced cardiac remodeling. The beneficial effects of ACE-inhibition have also been observed in growing children with asymptomatic valvular regurgitation; thus, it appears that the unloading therapy has the potential of influencing the natural history of both mitral and aortic regurgitation and possibly delays surgical valve repair or replacement. These data justify early inhibition of the renin-angiotensin system in children with left ventricular volume overload due to mitral and aortic regurgitation.
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PMID:New insights in the pathophysiology of mitral and aortic regurgitation in pediatric age: role of angiotensin-converting enzyme inhibitor therapy. 1125 36

Uncoupling proteins, inner mitochondrial membrane proton transporters, are important for regulating myocardial energy efficiency. We investigated the effects of the ACE inhibitor perindopril on cardiac performance, myocardial energy efficiency, and uncoupling protein expression in an aortic regurgitation rat model. Twenty male Sprague-Dawley rats, in which aortic regurgitation was produced, were divided into untreated and perindopril-treated (5 mg x kg(-1) x d(-1)) rats. The treatments were initiated 3 days after operation. Ten control rats were sham-operated. Measurements of blood pressure and echocardiography were repeated before and 100 days after operation (endpoint). Left ventricular uncoupling protein-2 expression, creatine phosphate, and adenosine triphosphate were measured at endpoint. In perindopril-treated rats, systolic and diastolic blood pressure decreased after treatment (92+/-4/65+/-2 mm Hg). At endpoint, left ventricular end-diastolic dimension in untreated (10.7+/-0.2 mm) and treated rats (9.2+/-0.2 mm) was increased, and fractional shortening was reduced in untreated rats (28+/-1%) but did not change in treated rats (36+/-2%). Uncoupling protein-2 mRNA expression increased in untreated rats (3.7-fold) and was suppressed by perindopril (1.5-fold). The creatine phosphate was reduced in untreated rats (10.6+/-0.7 micro mol/g) but not in treated rats (15.9+/-2.0 micro mol/g). In the chronic stage of aortic regurgitation, perindopril improved cardiac performance and myocardial energy efficiency, in which the suppression of uncoupling protein-2 may play an important role.
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PMID:Perindopril effect on uncoupling protein and energy metabolism in failing rat hearts. 1221 62

The efficacy of angiotensin-converting enzyme inhibitors (ACEIs) in the treatment of chronic aortic regurgitation (AR) is not well established and remains controversial. The mechanisms by which ACEIs may protect against left-ventricular (LV) volume overload are not well understood, and clinical trials performed until now have yielded conflicting results. This study was therefore performed to assess the effectiveness of two different doses of the ACEI captopril in a rat model of chronic AR. We compared the effects of a 6-month low-dose (LD) (25 mg/kg) or higher dose (HD) (75 mg/kg) treatment with captopril on LV function and hypertrophy in Wistar rats with severe AR. Untreated animals developed LV eccentric hypertrophy and systolic dysfunction. LD treatment did not prevent hypertrophy and provided modest protection against systolic dysfunction. HD treatment preserved LV systolic function and dimensions and tended to slow hypertrophy. The cardiac index remained high and similar among all AR groups, treated or not. Tissue renin-angiotensin system (RAS) analysis revealed that ACE activity was increased in the LVs of AR animals and that only HD treatment significantly decreased angiotensin II receptor mRNA levels. Fibronectin expression was increased in the LV or AR animals, but HD treatment almost completely reversed this increase. The ACE inhibitor captopril was effective at high doses in this model of severe AR. These effects might be related to the modulation of tissue RAS and the control of fibrosis.
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PMID:Angiotensin-converting enzyme inhibitor captopril prevents volume overload cardiomyopathy in experimental chronic aortic valve regurgitation. 1505 85

A 7-year-old girl was admitted because of dyspnea on exertion and palpitations. Her symptoms had gradually worsened for the last 6 months. She had physical features of the Marfan syndrome. Transthoracic echocardiography showed an ascending aortic aneurysm, severe aortic regurgitation, and mildly dilated left ventricle. Because of marked aortic aneurysm and severe aortic regurgitation, the patient was treated with a beta-blocker and an angiotensin converting enzyme inhibitor. Surgery was refused by her parents. We describe here a child with Marfan syndrome in whom significant dilatation of the ascending aorta and severe aortic regurgitation is encountered and major cardiovascular complications of Marfan syndrome were reviewed.
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PMID:Large ascending aortic aneurysm and severe aortic regurgitation in a 7-year-old child with Marfan syndrome and a review of the literature. Marfan syndrome in childhood. 1552 7


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