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)

Six double-blind studies were designed to assess the efficacy, tolerance, and safety of the angiotensin-converting enzyme inhibitor ramipril in patients with mild-to-moderate essential hypertension. Of 1,189 hypertensive patients in these studies, 105 patients were diabetic. They were randomly assigned either to a ramipril monotherapy group (1.25-10 mg/day) or to one of the following treatment groups: ramipril (5 mg/day) plus piretanide (3 mg/day), captopril (100 mg/day), enalapril (10-20 mg/day), hydrochlorothiazide (50 mg/day), or atenolol (100 mg/day). In all studies, a 4-week single-blind placebo run-in phase was followed by a 6-week double-blind active treatment phase. Significant reductions in blood pressure were achieved with all antihypertensive agents. No statistically significant deleterious effects were observed on concentrations of blood glucose, although diabetics who received hydrochlorothiazide showed slight increases in blood glucose levels. Ramipril was well tolerated by diabetic patients, and no serious adverse events occurred. Adverse events reported were typical of ACE inhibitors.
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PMID:Assessment of the efficacy, tolerance, and safety of ramipril in diabetic patients with mild-to-moderate hypertension: a retrospective analysis. 172 32

Exogenous obesity is characterized hemodynamically by expanded intravascular (plasma) volume associated with an increased cardiopulmonary volume and cardiac output. In contrast, essential hypertension is related to an increased total peripheral resistance that is more or less uniformly distributed throughout the component organ circulations associated with a contracted plasma volume in proportion to the height of arterial pressure. Thus, both cardiac output and total peripheral resistance are elevated in obesity hypertension, and both impose a load on the left ventricle, resulting in both a volume and a pressure overload left ventricular hypertrophy. Although renal vascular resistance is not as increased as it is in lean hypertensive patients, these patients are subjected to hyperfiltration and proteinuria. Additionally, these hemodynamic alterations coexist with carbohydrate intolerance, hyperinsulinemia, hyperlipidemia, and hyperuricemia. With weight reduction and associated pressure reduction, the hemodynamic and metabolic changes reverse toward normal. However, should this not be achievable, the angiotensin converting enzyme inhibitors and calcium antagonists provide rational physiological approaches to drug therapy. With these agents pressure reduction is achieved through a fall in vascular resistance without intravascular volume expansion, and this is associated with reduced left ventricular mass and preserved cardiac and renal function, and without exacerbation of preexisting metabolic perturbations. Hence, these two classes of antihypertensive agents may provide a rational and physiological means for reversing the pathophysiological alterations of hypertensive disease in those obese patients in whom weight control is not possible.
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PMID:Obesity hypertension. Converting enzyme inhibitors and calcium antagonists. 173 Apr 48

In experiments on rats, the physiological effects of the antihypertensive humoral system of the renal medulla were explored. We studied the parameters of blood pressure, heart rate, efferent sympathetic nervous activity to the splanchnic region, diuresis and natriuresis. The experimental situations included studies on normotensive rats, injected with extracted renomedullary lipids (medullipin), and normotensive rats extracorporally cross-perfusing an isolated kidney at increased pressure levels, to explore the release of renomedullary depressor substances. Spontaneously hyperactive rat (SHR) kidneys were also cross-perfused to study whether the renomedullary mechanism was reset upwards in this type of primary hypertension. Finally, the acute pressure reductions caused by angiotensin converting enzyme (ACE)-inhibitors were studied in intact and chemically medullectomized (2-bromo-ethylamine hydrobromide) rats to explore whether they were at least in part dependent on an intact renal medulla. In normal kidneys the renomedullary depressor system was initiated already at physiological pressure levels (at or above 100 mm Hg), causing the following humorally induced response pattern: the blood pressure fall was associated with decreases in both heart rate and sympathetic activity, while diuresis and natriuresis increased. In SHR kidneys, perfusion pressure had to be raised between 200 and 250 mm Hg before this depressor pattern was activated, revealing an "upward renomedullary resetting" well beyond the prevailing SHR blood pressure. The acute blood pressure decrease initiated in normotensive rats by an ACE-inhibitor (enalaprilat) was abolished in medullectomized rats, indicating an interaction between the renin-angiotensin and the renomedullary antihypertensive systems.
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PMID:Physiological effects of the humoral renomedullary antihypertensive system. 174 93

Late diabetic effects are the sequelae of for a long time super elevated blood sugar levels. The diabetic nephropathy is the cause of the secondary arterial hypertension. The investigation seeks for the connections between the diabetes mellitus and the essential, that is primary hypertension. The two diseases frequently appear and clearly increase in the second half of life. Moreover, they are above average frequently associated with each other. Among brothers and sisters of diabetic hypertensives in comparison to normal cohorts clearly increased high blood pressure prevalences were found. The insulin resistance which could be proved in a great number of hypertensive and which has been known since more than two decades might be the connecting link between hypertension and diabetes mellitus. Like the obesity the essential hypertension can be associated with all degrees of an insulin hyposensitiveness. The sodium-retaining effect of the insulin might explain the increased sodium content of the body in hypertensives. The differential diagnostics of the essential hypertension should therefore seek for conditions of an insulin resistance. The type II diabetic lacks a release of bradykinin during muscle work. Thus the glucose uptake into the cell is unfavourable influenced and demands an increased insulin excretion. This genetically (?) fixed defect is found also in essential hypertensives. It could be the connecting link between the two diseases. ACE-inhibitors have via a kininase II inhibition an effect also on the bradykinin decomposition and can favourable influence the glucose uptake into the muscle. An improved insulin effect among the ACE-inhibitors was described. Therefore, they should be preferred in the treatment of hypertensive diabetics.
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PMID:[Diabetes mellitus and arterial hypertension. In search of the connecting link]. 177 26

There are short-term and long-term modulations of cardiac function and cardiac composition by the endocrine and paracrine renin-angiotensin system. First, there is an enhancement of coronary vasoconstrictor tone in severe congestive heart failure due to stimulation of this system. Therapeutic interventions that block the RA-system are able to reduce the increased resistance to coronary flow. Second, there is a relationship between the occurrence of arrhythmias and the degree of sympathetic stimulation in congestive heart failure. The renin-angiotensin system may be involved in arrhythmogenesis because of presynaptic modulation of sympathetic neurotransmitter release. However, in the isolated perfused rat heart no class-specific antiarrhythmic properties could be found for ACE inhibitors during progressive myocardial ischaemia. Third, proliferation of the neointima following injury of a coronary artery is at least in part mediated by angiotensin II. Although ACE inhibition was an effective tool in animal experiments to prevent excessive proliferation of the neointima following ballooning, it was less effective in preventing restenosis in man following a repeat coronary angioplasty. Fourth, preferential proliferation of the cardiac interstitium in experimental hypertension has been associated with activation of the renin-angiotensin system. In patients with essential hypertension ACE inhibitors were not only capable of controlling blood pressure but also of normalizing the previously pathological pattern of diastolic left ventricular filling. In summary, by therapeutic intervention that cause a blockade of this system, cardioprotective and cardioreparative processes can be supported.
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PMID:Modulation of coronary circulation and the cardiac matrix by the renin-angiotensin system. 180 29

Short-term fluctuations in blood pressure and heart rate were analysed in a group of eight males with essential hypertension. Indirect finger blood pressure was measured by a non-invasive device (Finapres). Analogue-to-digital conversion of the blood pressure was used to determine systolic and diastolic blood pressure and heart rate every second. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transformation algorithm. The effect of 7-day administration of the angiotensin converting enzyme inhibitor, transolapril (2 mg/day), was assessed in a double-blind, randomized, placebo-controlled cross-over study. After trandolapril there was a significant reduction in systolic blood pressure levels (-15 mmHg). The reduction in diastolic blood pressure did not reach significance. The standard deviation of systolic and diastolic blood pressure levels were significantly reduced (-20% and -22% for systolic and diastolic respectively). Neither average heart rate nor standard deviations of heart rate time series was affected by the angiotensin converting enzyme inhibitor. Spectral analysis of fluctuation in blood pressure showed a reduction in the variability underlying the standard deviation changes of systolic and diastolic blood pressure. Trandolapril selectively reduced the amplitude of systolic and diastolic oscillations in the 66-129 mHz region, corresponding to Mayer waves. The significant decrease in the 10 s period oscillations of blood pressure after chronic angiotensin converting enzyme blockade with trandolapril could reflect reduced sympathetic outflow to vascular smooth muscle.
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PMID:Effects of the converting enzyme inhibitor trandolapril on short-term variability of blood pressure in essential hypertension. 182 64

Ramipril is a new, potent nonsulfhydryl inhibitor of angiotensin converting enzyme. The magnitude and duration of its antihypertensive effect were evaluated in a multicenter, placebo-controlled, randomized clinical trial conducted in 100 patients with mild to moderate essential hypertension. Ramipril significantly reduced both supine and standing blood pressures measured 24 h after dosing. Automated blood pressure monitoring showed that ramipril significantly reduced systolic and diastolic pressures for 24 h after dosing. The peak effect occurred between 3 and 6 h after dosing, with approximately 50% of this effect retained after 24 h. Ramipril was well tolerated; there was no significant difference between active drug and placebo in the overall incidence of side effects. Ramipril is an effective and well-tolerated antihypertensive agent, which reduces both supine and standing blood pressure over the entire 24-h period after dosing.
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PMID:24-hour blood pressure profiles in hypertensive patients administered ramipril or placebo once daily: magnitude and duration of antihypertensive effects. Ramipril Multicenter Study Group. 183 14

Cilazapril, an angiotensin converting enzyme (ACE) inhibitor with a long half-life, effectively reduced sitting diastolic blood pressure in patients with uncomplicated essential hypertension at dosages of 2.5, 5.0, and 10.0 mg/day, evaluated in a double-blind, placebo-controlled study. After a four-week placebo run-in period, 235 patients received either cilazapril or placebo for four weeks. At the end of the treatment period, significant decreases from baseline in sitting diastolic blood pressure were seen in all four groups (mean decreases of 3.3 mm Hg with placebo and 6.4, 9.2 and 8.3 mm Hg with 2.5, 5.0 and 10.0 mg cilazapril, respectively). The cilazapril groups had significantly greater blood pressure reductions than did the placebo group (p less than or equal to 0.02). The 5.0 mg cilazapril dose was significantly more effective than the 2.5 mg dose (p less than 0.03). The response rate was notably greater in the cilazapril treatment groups than in the placebo group (placebo, 27.5%; 2.5 mg cilazapril, 42.9%; 5.0 mg cilazapril 62.5%; 10.0 mg cilazapril, 50.0%). Cilazapril was well tolerated at all three dosages.
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PMID:Dose-finding study of cilazapril (Inhibace) in patients with uncomplicated essential hypertension. 183 86

The aim of this study was to determine the acute and chronic arterial effects of the ACE inhibitor, ramipril. Fourteen patients (mean age 47 years) with mild to moderate essential hypertension completed the study. A first haemodynamic examination was performed at the end of a 15-day placebo period (D15) before and 3 hours after oral administration of ramipril, 5 mg. Then all the patients started a 4-week treatment with ramipril, 5 mg/day. At the end of this period (D42) the haemodynamic examination was repeated 24 hours after the last capsule intake, and then 3 hours after administration of ramipril 5 mg. Brachial and carotid artery haemodynamics were evaluated by a bidimensional pulsed Doppler system. Arterial distensibility was non-invasively studied in three different arterial segments (carotido-femoral, brachio-radial, femoro-tibial) by the evaluation of the pulse wave velocity. Ramipril significantly decreased BP after acute or chronic administration. Chronic treatment with ramipril was followed by a long lasting increase in brachial artery diameter, a decrease in forearm vascular resistance, and an improvement in aortic distensibility. The other investigated arterial segments did not show any significant changes. Our results suggest that long lasting arterial effects of the ACE inhibitor ramipril are partly pressure-independent and are related to an effect of this drug on arterial tone. These effects may be able to reduce the hypertensive cardiac and arterial abnormalities.
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PMID:Long lasting arterial effects of the ACE inhibitor ramipril. 183 63

Cardiac hypertrophy in hypertension is related to increased peripheral vascular resistance and reduced aortic compliance. Non-invasive measurement of pulse wave velocities and systolo-diastolic variations of the diameter of the aortic arch show that an increase in the elastic modulus of the aorta is closely related to the increase in cardiac mass. This relationship holds even after correction for mean arterial pressure. Therefore, it has been suggested that, in hypertension, the decreased aortic compliance leads to a disproportionate increase in systolic blood pressure and end systolic wall stress, predisposing to cardiac hypertrophy. The blood pressure, arterial haemodynamics of the forearm (by pulsed Doppler flow measurement) and echocardiographic parameters were studied in 16 patients with permanent essential hypertension, before and 3 months after treatment with perindopril, an ACE inhibitor. In a simple blinded study versus placebo, perindopril was shown to significantly reduce the blood pressure (p less than 0.01) while brachial blood flow increased (p less than 0.01) because of a simultaneous increase in blood flow velocity and arterial diameter. During 5 minutes' occlusion at the wrist, blood flow velocity decreased more in patients taking perindopril than those on placebo (p less than 0.01) whilst the reduction in arterial diameter was equivalent, indicating that the increase in arterial diameter with perindopril could not be explained by flow-dependent dilatation alone but by a direct effect of the drug on the artery. During the treatment phase, brachial arterial compliance increased (p less than 0.01) and pulse wave velocity decreased (p less than 0.01) and there was no change in arterial shear stress defined as the product of mean blood pressure and arterial diameter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiac hypertrophy and arterial compliance after antihypertensive treatment]. 183 23


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