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 purpose of the study was to compare the effect of treatment with an angiotensin converting enzyme inhibitor (Lisinopril, MSD) or calcium blocker (Nifedipine retard, MSD) treatment during three months on blood pressure (measured with sphygmomanometric method and ambulatory blood pressure monitoring--ABPM) and urinary albumin excretion in essential hypertension class I acc. to WHO. Fifteen untreated patients aged 38 +/- 5 years with essential hypertension participated in the study and received diet with normal sodium content. Urinary albumin excretion was measured by RIA method in two 24 hour urine collections and mean value was calculated. ABPM was measured with Spacelabs monitor. After first examination 8 patients were randomly selected for the treatment with lisinopril and 7 patients to the treatment with nifedipine. The doses of both drugs were gradually adjusted to reach diastolic blood pressure below 90 mmHg. After 3 months of treatment urinary albumin excretion and blood pressure was found in both after treatment in patients treated with lisinopril but not in those receiving nifedipine. In patients treated with lisinopril a correlation between the decrease in systolic and diastolic blood pressure (measured by ABPM) and decrease of urinary albumin excretion was demonstrated. It was concluded that the normalization of blood pressure induced by lisinopril treatment in patients with uncomplicated essential hypertension and normoalbuminuria is accompanied with significant diminution of urinary albumin excretion which suggests preventive action of the drug in the development of microalbuminuria. Diminution of urinary albumin excretion caused by lisinopril is probably due to both the decrease of blood pressure and the specific renal action of the drug.
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PMID:[Comparison of treatment effects with an angiotensin converting enzyme inhibitor--lisinopril and a calcium blocker--nifedipine retard on urinary albumin excretion in patients with non-complicated essential hypertension]. 747 31

The aim of the investigation was to assess and compare the effects of a calcium channel antagonist, (i.e. amlodipine) and an ACE-inhibitor (i.e. lisinopril) in reducing chronic left ventricular hypertrophy in 15-week old spontaneously hypertensive rats (SHR). Changes in cardiac hypertrophy were assessed after 8 weeks by measuring the fractional rates of protein synthesis using a 'flooding dose' of [3H]-phenylalanine for 10 min. Blood pressure was monitored throughout the treatment period in both SHR and Wistar-Kyoto control rats (WKY). The results showed a decrease in blood pressure by amlodipine after 1 week of treatment which was further reduced at 4 to 8 weeks. Lisinopril caused immediate and sustained reductions in blood pressure (190 mmHg to 130 mmHg, P < 0.001). After 8 weeks of treatment in SHR rats, amlodipine had no significant effect on left ventricular weight (P > 0.05), whereas lisinopril caused a marked reduction. The protein content and RNA were also not changed by amlodipine. In contrast, lisinopril significantly lowered the tissue protein, RNA and DNA content (P < 0.001). The changes in the left ventricles of lisinopril-treated SHR rats were accompanied by an increase in the fractional synthesis rate of left ventricular myofibrillar proteins (+12 per cent, P < 0.025). The synthesis rate per unit RNA was also increased in right ventricular tissue of lisinopril-treated SHR rats. However, amlodipine had no effect on the fractional synthesis rates of any of the left-ventricular fractions of SHR rats (P > 0.05). The cellular efficiency in the right ventricle was also increased in amlodipine-treated SHR rats, indicating a moderate effect on protein metabolism. In conclusion, amlodipine had minimal effects in the reduction of established left ventricular hypertrophy (LVH), despite reducing the blood pressure, whereas lisinopril caused regression of LVH. These events were associated with small changes in protein synthesis rates, with the contractile protein showing an increase.
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PMID:Protein synthesis in the hypertrophied heart of spontaneously hypertensive rats and a comparison of the effects of an ACE-inhibitor and a calcium channel antagonist. 753 13

Thirty elderly, mildly hypertensive patients were enrolled for a single-blind, randomised cross-over placebo controlled trial in which placebo and lisinopril (20 mg/day before breakfast) were given for 4 and 8 weeks, respectively. A wash-out period of 3 weeks between placebo and lisinopril was observed. In each patient a euglycaemic glucose clamp with simultaneous indirect calorimetry allowed us to determine whole body glucose disposal and substrate oxidation. Changes in morning SBP and DBP were also determined. Lisinopril vs. placebo significantly improved whole body glucose disposal (40.4 +/- 0.4 vs. 30.3 +/- 0.4 mumol/kg LBM x min; P < 0.01), non-oxidative glucose metabolism (18.1 +/- 0.7 vs. 10.9 +/- 0.6 mumol/kg LBM x min; P < 0.01) and fasting plasma potassium levels (4.8 +/- 3 vs. 4.4 +/- 0.4 mmol/l; P < 0.05). SBP (175 +/- 3.3 vs. 160 +/- 3.0 mm Hg; P < 0.001) and DBP (106 +/- 2.3 vs. 95 +/- 2.0 mm Hg; P < 0.001) were significantly reduced by lisinopril administration. After ACE inhibition, fasting plasma potassium levels correlated with the decline in mean arterial BP (r = -0.71; P < 0.006). In conclusion, lisinopril administration reduces arterial BP and improves insulin sensitivity in elderly hypertensive patients.
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PMID:Lisinopril administration improves insulin action in aged patients with hypertension. 756 82

We wished to determine whether chronic treatment of rats with cyclosporin A (CSA), an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor antagonists modulates the angiotensin receptor density. In rats treated chronically with CSA, the vasoconstrictor response to angiotensin II (AII) is increased and this increase is modulated by ACEI and angiotensin receptor antagonists. Rats were treated for 6 weeks orally with CSA (15 mg/kg/day), the ACE inhibitor lisinopril (10 mg/kg/day), the angiotensin receptor antagonists DUP 753 (10 mg/kg/day), and D 8731 (10 mg/kg/day) and the combinations CSA + lisinopril, CSA + DUP 753, and CSA + D 8731. Olive oil was used as a control. The number of total AII receptors (Bmax) was determined by Scatchard analysis of [125I]Sar1 Ile8 AII binding in kidney, liver, adrenal cortex, and adrenal medulla. The receptor subtypes were analyzed with the specific antagonists DUP 753 (subtype 1) and PD 123319 (subtype 2). CSA upregulated angiotensin receptors in all organs studied. Lisinopril alone downregulated angiotensin receptors and abolished the effect of CSA in liver and adrenal cortex and medulla, but not in the kidney, where it had no effect. DUP 753 alone downregulated the angiotensin receptor subtype 1 in kidney, liver and adrenal cortex; its effect on the adrenal medulla in which 89% of angiotensin receptors are subtype 2, did not quite reach significance. The combination of DUP 753 and cyclosporin CSA abolished the CSA-induced increase in angiotensin receptor density in all four organs. The angiotensin receptor antagonists D 8731 downregulated the angiotensin receptors (subtype 1) in liver and kidney and upregulated angiotensin receptors (subtype 2) in the adrenal medulla.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue- and subtype-specific modulation of angiotensin II receptors by chronic treatment with cyclosporin A, angiotensin-converting enzyme inhibitors and AT1 antagonists. 756 68

In most, but not all, studies antihypertensive treatment with angiotensin converting enzyme inhibitors (ACE inhibitors) improves insulin sensitivity, whereas beta-blockers decrease insulin sensitivity. However, there was a significant increase in body weight with beta-blockers and changes in the body potassium homeostasis with ACE inhibitors. In order to compare the drug specific metabolic effects of an ACE inhibitor and a cardioselective beta-blocker controlling these factors, we measured insulin sensitivity in a randomized, double-blind cross-over study in 22 healthy volunteers (age 27 +/- 3 years; BMI 22.0 +/- 1.5 kg m-2 (mean +/- SD)) during euglycaemic glucose clamps before and after 4 weeks' administration of 5 mg Lisinopril or 5 mg Bisoprolol. Both drug phases were separated by 4 weeks of no drug administration. During the insulin sensitivity measurements potassium concentrations were clamped at basal levels by means of a variable i.v. potassium infusion. Body weight was monitored at weekly intervals and kept constant within +/- 1 kg of the subjects' baseline weight throughout the entire study period. Insulin sensitivity did not change significantly during either drug administration period. The insulin sensitivity index of the 22 volunteers after administration of the ACE inhibitor was 7.9 +/- 2.4 mL min-1 m2 microU-1 mL-1 (basal index 8.3 +/- 1.9 mL min-1 m2 microU-1 mL-1, and 7.5 +/- 2.1 mL min-1 m2 microU-1 mL-1 after administration of the beta-blocker (basal index 8.2 +/- 1.9 mL min-1 m2 microU-1 mL-1; NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Four week administration of an ACE inhibitor and a cardioselective beta-blocker in healthy volunteers: no influence on insulin sensitivity. 758 16

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 prognosis in patients with heart failure (HF) is poor. The angiotensin converting enzyme (ACE) inhibitors are among the most promising of current options, with benefits not only in terms of haemodynamic and clinical improvement but also in mortality. Data are reviewed comparing the once-daily ACE inhibitor lisinopril with captopril or enalapril in patients already receiving digoxin and/or diuretics for heart failure. Data are also reviewed which compare lisinopril with digoxin in patients already receiving diuretics alone for heart failure. Lisinopril is more effective than placebo and at least as effective as captopril or enalapril in these comparative studies on the basis of haemodynamics, exercise test results and clinical signs and symptoms of heart failure. Lisinopril may also be a suitable alternative, as well as being an adjunct, to digoxin in patients already receiving diuretics alone. Lisinopril is usually well tolerated in patients with heart failure. The mechanism of benefit of ACE inhibitors in heart failure is not clear, but apart from blockade of the renin-angiotensin-aldosterone system (RAAS), may also involve modulation of sympathetic stimulation, cardioreparation and regulation of potassium balance. The new ATLAS study (Assessment of Treatment with Lisinopril And Survival) is being conducted to address the question of whether ACE inhibitors in general practice should be given at the current low doses, or at the higher doses used in large survival studies.
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PMID:[Lisinopril in the treatment of heart insufficiency]. 766 80

Treatment with ACE inhibitors has improved the prognosis of cardiac failure (CF). The results of CONSENSUS I, SOLVD and V HEFT II show clinical improvement and longer survival with this therapeutic class of drugs. However, the search for the optimal dosage was not undertaken in these trials (a standard dose was fixed at the onset, average dose of enalapril from 15 to 20 mg/day). In clinical practice, patients are prescribed lower doses of ACE inhibitors (enalapril: 7.5 mg/day) than the averages used in large scale trials. In order to optimise the use of ACE inhibitors, the ATLAS study (Assessment of Treatment with Lisinopril and Survival) was undertaken with the precise objective of comparing two dosages (2.5 to 5 mg/day vs 32.5 to 35 mg/day) of lisinopril on the morbidity and mortality of patients with CF. This international, multicenter, randomised, double-blind parallel group trial aims to include 3,000 patients over 18 years of age with NYHA Classes II, III and IV, and an ejection fraction < or = 30% and to follow them up for 3 to 4.5 years. Nearly 30 French centres will participate in this trial. After an initial, open period of evaluation of tolerance (5 mg to 15 mg/day of lisinopril in France), the patients will be randomised to two groups. After randomisation, all patients will receive 5 mg per day of lisinopril. The "high dose" group will receive 20 mg/day for two weeks, then 30 mg/day in addition to the "open dosage". In cases of intolerance, the dosage may be reduced to 20 mg/day or 10 mg/day, or the drug may be withdrawn.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The ATLAS study (Assessment of Treatment with Lisinopril and Survival); justification and objectives]. 786 22

Plasma concentration of two main cardiovascular substances - atrial natriuretic factor (ANF) and endothelin - were studied in control subjects (n = 21) under basal conditions and 90 minutes after oral administration of glucose. In hypertensive patients (n = 21) these determinations were repeated after 12 weeks treatment with an angiotensin I-converting enzyme inhibitor lisinopril (Prinivil, Merck Sharp and Dohme). While basal and post-glucose ANF concentrations did not differ in controls and hypertensive patients, a tendency to the higher endothelin levels was found in our group of essential hypertension when compared to normotensive subjects. Glucose loading did not change significantly ANF concentrations in any studied group but significantly lowered plasma endothelin in both controls (from 13 +/- 0.95 to 9.50 +/- 0.95 fmol/ml) and hypertensive patients (from 15.05 +/- 1.23 to 12.15 +/- 1.03 fmol/min). Treatment of hypertensive patients with lisinopril paradoxically increased concentrations of ANF (from 6.43 +/- 2.53 to 11.47 +/- 4.90 fmol/ml) and lowered that of endothelin (from 15.05 +/- 1.23 to 12.17 +/- 1.58 fmol/ml). From our findings we may suggest that the relative predominance of the vasoconstrictor (endothelin) over the vasodilator (ANF) humoral substances might participate in pathogenesis of EH and that the reversal of this disadvantageous ratio after lisinopril (increase of ANF and decrease of endothelin) might contribute to the blood pressure reducing effect of ACEI. The drop in plasma endothelin after glucose remains so far unexplained consequence of glucose loading in both control and hypertensive subjects.
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PMID:Plasma concentrations of some cardiovascular humoral factors in essential hypertension and their changes during the treatment with converting enzyme inhibitor lisinopril. 799 8

Arterial hypertension is nowadays no longer considered an isolated disorder of blood pressure regulation but a multifactorial disease with metabolic and cellular deviations. From the therapeutic aspect of thus conceived hypertension today inhibitors of the angiotensin converting enzyme seem most promising. With regard to their assumed comprehensive effect, the authors investigated simultaneously selected pressor and depressor humoral indicators and other indicators in 21 hypertensive patients with stage I and II of essential hypertension before and after three-month treatment with an angiotensin converting enzyme inhibitor lisinopril (Prinivil, Merck, Sharp and Dohme) and compared them with findings in 21 normotensive healthy subjects. Hypertensive subjects before treatment had, as compared with normotensives, significantly lower urinary kallikrein (7.8 +/- 1.2 < 18.0 +/- 4.2 EU/24hr, a significantly higher basal plasma adrenalin (1.27 +/- 0.20 > 0.54 +/- 0.20 pmol/ml) and adrenalin after a glucose load (1.26 +/- 0.22 > 0.51 +/- 0.12) and a higher relative plasma viscosity (1.74 +/- 0.02 > 1.67 +/- 0.01). The two groups did not differ significantly as to the plasma renin activity, plasma aldosterone and fibrinogen concentration and the level of urinary prostaglandins per 24 hr: 6-keto-prostaglandin F1a, thromboxane B2 and prostaglandins E and F2a. The 75 g glucose load produced an increased plasma renin, aldosterone and noradrenaline activity in normotensives as well as hypertensives before and after lisinopril treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in humoral pressor and depressor factors in essential hypertension during lisinopril therapy]. 802 67


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