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)

Serum levels of angiotensin converting enzyme (SACE) were measured in 118 diabetic patients divided into the following four groups: 44 insulin-treated diabetic patients with severe retinopathy, 38 non insulin-treated diabetic patients with severe retinopathy, 18 diabetic patients, including both insulin-treated and non insulin-treated subjects with background retinopathy, 18 diabetic patients, insulin-treated and non insulin-treated without signs of retinopathy. Nineteen retinopathic patients non diabetic were also studied in order to verify whether SACE levels are altered when retinopathy is present independently from diabetes. The control group was composed of 44 normal subjects. When the data from the above six groups of subjects were submitted to statistical tests (one-way ANOVA, T-test of Bonferroni and test of Student-Newman-Keuls), the study yielded the following results: i) a remarkable difference between the SACE levels in healthy subjects and those in the three groups of diabetic retinopathic patients considered; ii) a non statistically significant difference of SACE levels between normal subjects and diabetic patients without retinopathy; iii) a non statistically significant comparison of SACE levels of normal subjects versus non diabetic retinopathic patients. Therefore, we concluded that while primitive diseases of the retina are not associated with an increase of SACE levels, yet when diabetes and retinopathy coexist, the SACE levels increase remarkably (in rather an independent way from the type of diabetes, the age of subjects, the stage of retinal disease and the daily average insulin dose), suggesting that most of the enzyme's increase originates from the endothelium of peripheral vasa, widely involved in most of the retinopathic diabetic patients.
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PMID:Serum angiotensin converting enzyme in diabetic retinopathy. 133 20

We assessed blood pressure and neurohumoral factors at rest and during exercise in 10 patients with essential hypertension before and after treatment with the new angiotensin converting enzyme inhibitor, alacepril (25-50 mg day-1). Alacepril significantly lowered mean blood pressure at rest and at the same exercise load as before treatment without affecting heart rate response. The response of plasma renin activity, plasma aldosterone, and plasma adrenaline were not changed by alacepril, but increase of plasma angiotensin II and plasma noradrenaline during exercise were significantly attenuated after alacepril treatment (ANOVA, P = 0.04, both). The change in mean blood pressure during exercise was positively correlated with the decrease in plasma angiotensin II (r = 0.65, P < 0.05). These results demonstrated that alacepril was effective in essential hypertension both at rest and during exercise, suggesting that the antihypertensive effect during exercise might be related to the decrease in pressor hormones, especially in plasma angiotensin II.
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PMID:Effect of alacepril on blood pressure and neurohumoral factors at rest and during dynamic exercise in patients with essential hypertension. 145 72

The hypotensive and hormonal effects of the angiotensin converting enzyme (ACE) inhibitor enalapril (10 mg twice daily) were compared with those of hydrochlorothiazide (25 mg twice daily), with the two drugs in combination and with placebo in 21 patients with essential hypertension. For each patient there were four randomised double-blind treatment phases, each of four weeks' duration, which comprised a 2 X 2 factorial experiment. All blood pressure parameters were reduced in the three active treatment phases compared to placebo (p less than 0.001). Supine mean blood pressures were 119 mmHg (placebo), 113 mmHg (hydrochlorothiazide), 108 mmHg (enalapril), and 98 mmHg (hydrochlorothiazide plus enalapril) (SEM 3 mmHg, ANOVA). Enalapril and hydrochlorothiazide were equally effective and well tolerated and their hypotensive effects were additive. Enalapril increased plasma renin activity (PRA), reduced plasma angiotensin II (AII) and aldosterone concentrations, and reduced ACE activity, whereas hydrochlorothiazide increased PRA, plasma AII, and aldosterone concentrations without altering ACE activity. With combination treatment the effects of enalapril on PRA and plasma AII concentrations were potentiated whereas those on plasma aldosterone concentration and ACE activity were additive. Atrial natriuretic factor plasma concentration in the placebo phase was 92 pg/ml and increased to 145 pg/ml in the hydrochlorothiazide phase (p less than 0.001, SEM 13 pg/ml), but there was no significant change in either the enalapril or combination phases.
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PMID:Effects of enalapril and hydrochlorothiazide on blood pressure, renin-angiotensin system, and atrial natriuretic factor in essential hypertension: a double blind factorial cross-over study. 302 94

In order to evaluate the effect of the angiotensin I-converting enzyme inhibitor, captopril, on lipid metabolism, we measured serum lipoperoxides concentration ( LPX ) as well as plasma levels of renin activity (PRA), aldosterone (PAC) and bradykinin ( PBK ) before and after captopril administration in 15 hypertensive patients. Captopril significantly lowered the LPX (p less than 0.05 by repeated measures ANOVA) from the control value of 3.25 +/- 1.16 (mean +/- S.D.) to 2.92 +/- 0.94, 2.83 +/- 1.10, and 2.89 +/- 1.31 nmol/ml 30, 60, and 120 min after the administration, respectively. A significant reduction of blood pressure (p less than 0.0001) and PAC (p less than 0.01) was observed following captopril administration, while PBK increased significantly (p less than 0.001) from a baseline level of 10.85 +/- 4.07 to 13.95 +/- 5.29, 16.25 +/- 6.85, and 15.71 +/- 7.65 pg/ml 30, 60, and 120 min after captopril administration, respectively. There was no significant correlation between changes in serum LPX and in mean blood pressure, PRA and PAC, though a significant inverse relationship was found between changes in serum LPX and in PBK 120 min after the administration (r = -0.576, p less than 0.05, n = 13). Although the mechanisms by which serum LPX is decreased by captopril are not clear, it is suggested from the results that captopril is a beneficial antihypertensive agent for preventing LPX -induced atherosclerosis in hypertensive patients.
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PMID:[The effects of the angiotensin I-converting enzyme inhibitor, captopril, on serum lipoperoxides level and the renin-angiotensin-aldosterone and kallikrein-kinin systems in hypertensive patients]. 637 99

Hypertensive patients undergoing hemodialysis (HPH) have a marked impairment of their large artery distensibility and an increased cardiovascular morbidity. We investigated twelve HPH (8 males, 4 females, 53 +/- 12 years of age, +/- SD) following a single dose of an ACE inhibitor (quinapril 20 mg) comparatively to a placebo in a randomised cross over study over a week (H0 to H172). We measured repeatedly blood pressure and aortic distensibility (carotid-femoral pulse wave velocity, PWV). Statistical analysis was made through repeated measure ANOVA and repeated measure analysis of covariance because of the tight link between pressure and arterial function. Blood pressure decreased (SAP: p < 0.01, DAP: p < 0.001), and PWV was significantly improved independently of the pressure decrease. ACE inhibitor reduces blood pressure in these patients and improves large arterial function independently of the blood pressure changes.
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PMID:[Pressure-independent improvement of aortic distensibility in hypertensive hemodialysed patients]. 775 59

Pharmacokinetic interaction between benazepril (ACE inhibitor) and amlodipine (calcium channel blocker) was studied in 12 healthy subjects. Single doses of benazepril hydrochloride (10-mg tablet) and amlodipine besylate (tablet equivalent to 5 mg amlodipine) were administered alone or in combination according to a three-way, Latin-Square, randomized cross-over design. Serial blood samples were collected following each administration for the determination of benazepril and its active metabolite benazeprilat and amlodipine. The mean values of AUC (0-4 h), Cmax and Tmax for benazepril given as combination versus given alone were 161 vs 140 ng.h.ml-1, 168 vs 149 ng.ml-1, and 0.5 vs 0.6 h. The mean values of AUC (0-24 h), Cmax and Tmax for benazeprilat after benazepril given as combination versus given alone were 1470 vs 1410 ng.h.ml-1, 292 vs 257 ng.ml-1, and 1.7 vs 1.5 h. The mean values of AUC (0-144 h), Cmax and Tmax for amlodipine given as combination versus given alone were 118 vs 114 ng.h.ml-1, 2.5 vs 2.3 ng.ml-1, and 8.3 vs 9.0 h. The differences in these pharmacokinetic parameters between the combination and monotherapy treatments were not statistically significant based on ANOVA. The results of this study indicate that no pharmacokinetic interaction existed between the two drugs.
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PMID:Pharmacokinetic interaction study between benazepril and amlodipine in healthy subjects. 786 83

1. The association of alleles of an insertion/deletion polymorphism (I/D) of the dipeptidyl carboxypeptidase-1 gene with hypertension is controversial. If a particular allele makes a major contribution to blood pressure, then hypertensives homozygous for this allele could be expected to have higher high blood pressure than those homozygous for the alternate allele. 2. The present study examined this hypothesis by comparing pretreatment blood pressures of hypertensives who had been genotypes for the I/D polymorphism. Blood pressures for different age groups (< 50, 50-59 and > or = 60 years) were also examined for each genotype. In addition, several other parameters were examined. 3. Systolic blood pressures were found to be 167 +/- 3, 167 +/- 3 and 170 +/- 6 mmHg (mean +/- s.e.) for the genotypes II, ID and DD, respectively. Diastolic blood pressures were 113 +/- 4, 111 +/- 2 and 111 +/- 4, for the respective genotypes. One-way ANOVA showed that the respective blood pressure values did not differ significantly across genotypes. Blood pressures for different age groups of hypertensives were also similar. 4. In addition, body mass index, mean age and sex did not differ between genotypes, either for the group as a whole or for the different age groups. 5. In conclusion, the present study could find no evidence to support a genetic association between the I/D polymorphism of DCP1 and blood pressure in a group with severe, familial hypertension living in Sydney.
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PMID:Similarity of blood pressure for each genotype of the insertion/deletion polymorphism of the dipeptidyl carboxypeptidase-1 gene in different age groups of patients with severe, familial essential hypertension. 788 86

There have been no studies of the possibility of reversing the left ventricular hypertrophy (LVH) of chronically hemodialyzed hypertensive uremics (HDH) with long-term antihypertensive therapy. We have measured left ventricular sizes of eight (6 male, 2 female, aged 29 to 61 years) HDH with M-mode echocardiography, before and 12, 18 and 24 months after the start of a combined antihypertensive therapy which included ACE-inhibitors, beta-blockers and calcium-antagonists. Pre-treatment values for mean blood pressure (MBP), 116.6 +/- 2.9 mm Hg, end diastolic diameter (EDD), 62.6 +/- 6.6 mm, interventricular septum (IVS), 14.2 +/- 3.0 mm, and left ventricular mass index (LVMi), 239 +/- 61 g/m2, were all significantly higher than those for nine sex- and age-matched hemodialyzed normotensive subjects (HDN) with comparable hemoglobin (Hb) levels. During the antihypertensive treatment, both the systolic and diastolic BP decreased steadily (P = 0.0001; P = 0.0003; ANOVA) and significantly by the third month (P < 0.05; P < 0.01), reaching levels comparable to those of the HDN group after 12 months. At this time the LVMi (204 +/- 67) and the IVS (13.1 +/- 2.7), although both significantly lower than baseline, were still higher than in the HDN group, while the EDD was similar. After 24 months, however, both the IVS (12.3 +/- 3.1) and the LVMi (161 +/- 65) were no longer different from those of the HDN group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regression of left ventricular hypertrophy in hypertensive dialyzed uremic patients on long-term antihypertensive therapy. 825 65

1. The effects of genetic factors on cardiac myocyte diameter and other phenotypes of heart size were determined in genetically hypertensive rats. Direct blood pressure, heartweight and cardiac myocyte size were measured at 12 weeks of age in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats and F2 males derived from these rats. The genotypes of the angiotensin converting enzyme (ACE) gene on rat chromosome 10 were determined by amplification of DNA using the polymerase chain reaction in F2 animals and were correlated with measures of phenotypes using ANOVA and t-test. 2. Significant correlations between fibre diameter and myocytes and heartweight or left ventricular weight were observed in SHR, WKY and F2 males. There was no correlation of myocyte size with systolic blood pressure in F2 rats. ACE genotype was weakly correlated with heartweight, but not correlated with myocardial fibre diameter in F2 males, suggesting that this gene may primarily cause expansion of extracellular tissue rather than cardiac myocyte size. 3. Genetic factors may influence heart size through effects on the cardiac myocyte or connective tissue elements. Our results suggest that the growth of myocardial fibres and the increase in volume of interstitial elements in the hypertrophic heart are under independent genetic control.
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PMID:Analysis of linkage of the ACE locus with measures of cardiac hypertrophy in the spontaneously hypertensive rat. 880 May 96

The effects of chronic treatment with the specific AT1 angiotensin receptor antagonist, irbesartan, or the angiotensin converting enzyme inhibitor, enalapril, were assessed in uninephrectomized fawn-hooded hypertensive rats (FHH) and compared with vehicle treatment. Three days after uninephrectomy, irbesartan (240 mg/liter), enalapril (80 mg/liter) or vehicle were administered via the drinking water. Systolic blood pressure (SBP) and protein excretion rates (UprotV) were determined monthly. In rats receiving irbesartan (N = 7) and enalapril (N = 6) SBP (132 +/- 3 mm Hg and 133 +/- 6, respectively) was essentially normalized at 12 weeks when compared with vehicle (169 +/- 6 mm Hg (N = 6); all comparisons were P < 0.05 by ANOVA). Similarly, proteinuria was lower in irbesartan (44 +/- 12 mg/day) and enalapril (19 +/- 2) groups versus vehicle (123 +/- 10 mg/day). Treatment with both drugs was associated with marked reduction in glomerulosclerosis at 12 weeks (both < 5% vs. vehicle, 43 +/- 9%) without effect on glomerular volume. In identically prepared rats, glomerular capillary hydraulic pressure (PGC, estimated from stop-flow pressure, Psf) was lower in FHH receiving irbesartan (58 +/- 1 mm Hg, N = 6) or enalapril (54 +/- 2, N = 6) than in vehicle-treated rats, in whom PGC was greatly elevated (68 +/- 2 mm Hg; N = 7). Despite this, GFR and single nephron GFR were well maintained. These data support a critical role for AT1 receptor-mediated, angiotensin-dependent processes in the pathogenesis of hypertension in FHH, and further implicate elevated PGC as a major determinant of glomerular injury in this model.
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PMID:The angiotensin receptor antagonist, irbesartan, reduces renal injury in experimental chronic renal failure. 894 34


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