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 aim of the study was to analyze changes in myocardial angiotensinogen gene expression and myocardial angiotensin converting enzyme activity in slowly progressing low-output failure. In adult, male Wistar rats, acute ventricular tachypacing by 610 to 620 impulses per minute lowered end-diastolic external diameter of the left ventricle by 2.6% (p less than 0.01), but did not lower cardiac output or abolish coronary reserve, since left-ventricular subendocardial blood flow of paced rats increased under dipyridamole (2 mg/kg i.v.) by 56% (p less than 0.01). Systemic neuroendocrine activation and ventricular dilation without enlargement of ventricular mass developed subsequent to chronic tachypacing, but left-ventricular diameter during pacing never exceeded the value of sham rats on sinus rhythm. After 2 weeks, cardiac output was lowered by 14% (p less than 0.001), cardiopulmonary blood volume was elevated by 30% (p less than 0.001), and angiotensinogen mRNA and angiotensin converting enzyme activity in ventricular myocardium were doubled. We conclude that conditions for an enhanced intracardiac angiotensin II-formation developed in tachypacing-induced heart failure, but that enhanced systolic wall stress or myocardial ischemia are not required for this activation of the local cardiac renin-angiotensin system.
Basic Res Cardiol
PMID:Enhanced cardiac angiotensinogen gene expression and angiotensin converting enzyme activity in tachypacing-induced heart failure in rats. 165 3

Ambulatory blood pressure and heart rate monitoring were used for comparing the antihypertensive effect of a 1-week treatment with enalapril and lisinopril 10 mg once daily (double-blind crossover placebo-controlled study). Twelve outpatients with mild to moderate hypertension were treated. Both drugs had a significant and identical hypotensive effect. Neither drug affected the diurnal rhythm of blood pressure or heart rate. Therefore the two drugs are equipotent antihypertensive agents. Both drugs inhibited ACE activity to a highly significant extent, but in this regard lisinopril was more effective than enalapril. However, lisinopril's greater ACE inhibition was not accompanied by a greater hypotensive effect. The clinical value of this difference is not yet established.
Clin Cardiol 1991 Nov
PMID:Different hemodynamic (24-h ambulatory blood pressure monitoring) and renin-inhibiting effect of a 1-week treatment with enalapril and lisinopril. 166 62

The left ventricle of the neonatal pig heart is a model of rapid physiological cardiac growth that is dependent upon accelerated ribosome formation and increased RNA content. The goals of the present study were to investigate the role of angiotensin II in this rapid growth. Hearts from 3 d old control piglets or piglets that were treated with enalapril maleate, an angiotensin converting enzyme inhibitor, or DuP 753, an angiotensin II receptor antagonist, were used for measurements of left ventricular mass, RNA, DNA and protein. Hearts from enalapril-treated pigs also were used for measurements of rates of ribosome formation and total protein synthesis during perfusion as modified Langendorff preparations. Treatment of piglets with enalapril maleate resulted in decreased left ventricle/body wt ratio, RNA content, total RNA and total protein in the left ventricle. These parameters were unaffected in the right ventricle. In vitro perfusion of hearts from enalapril-treated piglets revealed decreased ribosome formation and total protein synthesis in the left ventricle. Piglets treated with DuP 753 had decreased left ventricle/body wt ratio as well as decreased RNA content, total RNA and RNA/DNA ratio in the left ventricle. These results suggest that angiotensin II may be required for rapid growth of neonatal pig hearts.
J Mol Cell Cardiol 1991 Sep
PMID:Angiotensin II and left ventricular growth in newborn pig heart. 171 24

Angiotensin-converting-enzyme inhibitors are frequently used in conjunction with diuretics in the treatment of congestive cardiac failure. We report two cases in which use of a proprietary combination diuretic containing a loop diuretic and potassium sparing agent with an angiotensin converting enzyme inhibitor was associated with hyperkalaemic cardiac arrest. Successful resuscitation from the arrest permitted elucidation of its mechanism. We believe that this outcome has not previously been reported, and emphasise the importance of electrolyte monitoring in patients receiving angiotensin converting enzyme inhibitors particularly if prescribed in addition to fixed combination proprietary diuretics.
Int J Cardiol 1992 Feb
PMID:Preventable sudden death in patients receiving angiotensin converting enzyme inhibitors and loop/potassium sparing diuretic combinations. 173 74

Attempts at treating idiopathic cardiomyopathy have been made both clinically and experimentally using the cardiomyopathic Syrian hamster. In recent years, the angiotensin converting enzyme (ACE) inhibitor has attracted considerable attention as an agent to treat heart failure. We administered the ACE inhibitor captopril to the cardiomyopathic hamster. In this study, 15 mg/kg body weight of captopril was administered to the cardiomyopathic hamster J2N at 5 weeks of age for 10 weeks; age matched J2N hamsters were used as non-treated control animals. At the end of captopril administration, blood was collected from the ventral aorta. Serum malondialdehyde (MDA), serum CPK, aldolase and LDH were determined, and myosin isoenzyme patterns of the extirpated myocardium were compared. Additionally, ECGs were compared and the fibrotic ratio of both ventricles determined. Serum MDA, CPK, and aldolase increased significantly in the cardiomyopathic hamster, whereas these indices were significantly inhibited in the hamster treated with captopril. The pathological ECG findings and the ventricular V3 predominant myosin isoenzyme patterns of the J2N were also much improved in the captopril group. However, the improvement in these parameters by enalapril administration was less than that seen with captopril. These results suggested that the effect of captopril is not only due to decrease of the angiotensin II level, but also due to increase in tissue kinin and vasodilatory prostaglandin which play an important role in the beneficial effect of captopril.
Basic Res Cardiol 1991
PMID:Protective effect of ACE- and kininase-inhibitor on the onset of cardiomyopathy. 178 64

We prospectively studied 69 consecutive patients hospitalized with a primary diagnosis of acute left ventricular failure so as to assess the impact of vasodilators on incidence and morbidity of acute symptomatic left ventricular failure. The determinants of duration of hospitalization, in-hospital mortality and symptomatic status 2 months after discharge were examined. There were 9 in-hospital deaths (13%), and survival at 60 days was 77%. Median duration of hospitalization was 9 days, and 33% of the surviving patients remained in New York Heart Association functional class III-IV 60 days subsequent to discharge. Of the patients, 49 (76%) had previously received treatment for left ventricular failure: 30 (61%) of these had received vasodilators, most commonly angiotensin converting enzyme inhibitors and nitrates. Ischaemic chest pain was present in 34 (49%) of the patients. Acute utilization of vasodilators (45% of patients) was largely limited to nitrate therapy associated with ischaemic chest pain (P less than 0.01). Multiple logistic regression revealed previous left ventricular failure, advanced age and hypokalaemia as significant correlates of prolonged hospitalization (greater than 9 days). Previous left ventricular failure was also predictive of persistent severe disability two months subsequent to discharge. No factor was a significant predictor of in-hospital death. Although preceding treatment with digoxin and incremental angiotensin converting enzyme inhibitor therapy tended to predict brief hospitalization, the parameter of acute ischaemia, other biochemical anomalies and modes of acute or chronic therapy were not significant correlates of any end point. We conclude that preceding disability, rather than mode of treatment, predicts an adverse outcome in acute left ventricular failure.
Int J Cardiol 1991 Sep
PMID:Acute heart failure: determinants of outcome. 179 Oct 90

Vasodilators have been shown to improve hemodynamics of the failing heart as a short-term effect, and to decrease mortality as a long-term result. We, therefore, studied the effects of vasodilators and inotropic agents on myocardial mechanics and energetics in patients with congestive heart failure New York Heart Association (NYHA) classes II-III. In these patients, who underwent routine heart catheterization, myocardial oxygen consumption was measured using the argon method, and LV pressure and geometry were obtained from LV angiography using a Millar microtipped catheter. All data were analyzed for one single heart beat. The best correlation was found between MVO2/beat and the systolic stress-time integral which considers LV pressure, LV wall thickness, and LV geometry. The relation between MVO2/beat and peak systolic wall stress was less relevant. No correlation was found between MVO2/beat and pressure-volume work, dP/dtmax, and mean velocity of circumferential fiber shortening. The intravenous application of nitroprusside and the ACE-inhibitor benazepril decreased both the systolic stress-time integral and the myocardial oxygen consumption in proportion to each other, indicating unchanged economy of myocardial contraction. In contrast, beta 1-agonists and phosphodiesterase inhibitors increased myocardial oxygen consumption independently of changes in the stress-time integral. In conclusion, vasodilators decrease LV pressure and chamber size and thereby proportionally reduce MVO2/beat. The reduction of energy needed for myocardial contraction may partially explain the long-term effects of the ACE-inhibitors and combinations of vasodilators. Pure inotropic substances, especially beta 1-agonists, increase myocardial oxygen consumption with only minor changes of systolic stress-time integral.(ABSTRACT TRUNCATED AT 250 WORDS)
Basic Res Cardiol 1991
PMID:Energetic consequences of substances currently used or recommended for long-term treatment of chronic heart failure. 182 77

Eleven patients with congestive heart failure class II-IV (NYHA) caused by ischemic heart disease were studied before and three months after adding enalapril to their treatment with furosemide. After an infarction the heart dilates gradually, mainly as a result of slippage of myocardial fiber bundles. It is known that the addition of an ACE-inhibitor to the medical treatment unloads the heart and gradually, within a period of 3 months, reduces heart size. Objectives of this study were to demonstrate remodelling by recording diastolic pressure-volume relations before and after treatment. The study addresses the question of whether regression of dilation, induced by the ACE-inhibitor treatment, improves the oxygen supply-demand ratio and, as a result, the contractility of the heart muscle. Treatment resulted in a reduction of vascular resistance (1479 to 1182 dyn.s.cm-5, p less than 0.05) and of the left ventricular end-diastolic (130 to 108 ml per m2 body surface area, p less than 0.05) and end-systolic (102 to 81 ml per m2 body surface area, p less than 0.01) volume index. The slope of the end-systolic pressure-volume relation, measured using vena cava occlusion and beat-to-beat recording of pressure and volume loops, remained unchanged. Indices of oxygen-supply demand ratio such as a drop of ejection fraction during exercise and parameters of active diastolic relaxation also did not change. Addition of an ACE-inhibitor induces regression of ventricular dilation, but no indications were found that it improves the condition of the cardiac muscle.
Basic Res Cardiol 1991
PMID:Cardiac remodelling and myocardial contractility in patients with congestive heart failure treated with furosemide and enalapril. 182 82

It has been shown that converting enzyme inhibitors (CEI) attenuate ventricular dilatation and hypertrophy after myocardial infarction. In most studies, CEI treatment was started when ventricular dilatation and hypertrophy were already well under way. Therefore, we studied the effects on ventricular dilatation and hypertrophy, when CEI treatment was started in the acute phase of myocardial infarction. Immediately after a sham-operation or myocardial infarction in rats (sham: n = 8; MI: n = 17), treatment with zofenopril, a novel ACE-inhibitor, was started and continued during 42 days (long-term treatment). In a second group of rats, zofenopril was administered only during the first 5 days after myocardial infarction (short-term treatment); these rats were not treated with zofenopril during the remaining period of 37 days (sham: n = 5; MI: n = 13). Untreated rats served as controls (sham: n = 9; MI: n = 24). The results from this study showed that long-term treatment with zofenopril caused a significant reduction of left ventricular cavity volume in rats with moderate-to-large infarctions, which was accompanied by a significant reduction in the ratio of total heart weight to body weight. However, short-term treatment with zofenopril did not significantly reduce ventricular volume or total heart weight. Finally, both long- and short-term treatment resulted in a small, but statistically significant, reduction of septal wall thickness in sham-operated and infarcted rats. We conclude that CEI therapy decreases ventricular dilatation and hypertrophy after myocardial infarction, only when treatment is continued during the chronic phase.(ABSTRACT TRUNCATED AT 250 WORDS)
Basic Res Cardiol 1991
PMID:The effects of short- and long-term treatment with an ACE-inhibitor in rats with myocardial infarction. 182 83

Hemodynamic and structural changes of the heart and large arterial vessels were studied in normotensive and spontaneously hypertensive rats following 12-week administration of converting enzyme inhibitor (perindopril, 2 mg/kg daily by gavage). In both strains, a significant blood pressure reduction was observed. In normotensive rats, the hemodynamic changes involved significant increase in systemic arterial compliance, whereas slight changes in left ventricular weight and aortic medial thickness were observed. In hypertensive rats, the increase in compliance was relatively small, whereas there was a major reduction in medial thickness. The reduction of the media thickness was much more pronounced than that of the left ventricular hypertrophy. In both strains, the collagen density in the subendocardial layers of the left ventricle was significantly decreased in treated vs untreated groups. The isomyosine profile of the left ventricular muscle was also modified by ACE inhibition with an increase in the V1 form and a decrease in the V3 form. The present results suggest that the cardiac and arterial changes observed following long-term converting enzyme inhibition do not strictly parallel the blood pressure changes in hypertensive rats. Dissociation between cardiac and arterial changes may be observed.
Basic Res Cardiol 1991
PMID:Angiotensin converting enzyme (ACE) inhibitors in experimental hypertension: influence on heart and arteries. 182 84


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