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)

Male weanling Wistar rats received 200 micrograms/ml of mercury (Hg), as HgCl2, in drinking water for 180 days. At the end of the treatment, systemic arterial blood pressure was augmented, cardiac inotropism was reduced, and heart rate was unchanged. Light and electron microscopical studies of the kidney showed a mesangial proliferative glomerulonephritis in about 80% of the glomeruli. Tubular cells showed reduction of the acid phosphatase activity, which was related to functional abnormalities of the lysosomes. In the 24 hour urine samples of the Hg exposed rats, there was slight reduction of kallikrein activity, but evident proteinuria was not present in all samples. Plasma renin activity was reduced, that of angiotensin I-converting enzyme was augmented, and plasma aldosterone concentrations were unchanged. Mercury was accumulated mostly in the kidney of the Hg treated animals; and the content of Hg in the heart was higher than in the brain. These data show that chronic exposure to Hg acts on the kidney with complex mechanisms of toxicity; these contribute to modify systemic haemodynamics.
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PMID:Renal mechanisms in the cardiovascular effects of chronic exposure to inorganic mercury in rats. 157 Dec 92

It has been suggested that angiotensin converting enzyme (ACE) may play a role in the metabolism of atrial natriuretic peptide (ANP), and that ANP may interfere with angiotensin-induced vasoconstriction. This has been investigated within the forearm vascular bed during local ANP infusion and ACE inhibition. Six normotensive volunteers were studied, each on two occasions. On both occasions, after saline infusion, volunteers were given initially a 20 min infusion of ANP at 0.1 microgram/min via the brachial artery. This was followed, after 20 min, by a second infusion of ANP at the same dose, co-infused with enalaprilat (5 micrograms/min) on one occasion, and placebo (saline) on the other (in random order). Forearm blood flow was measured using venous occlusion plethysmography with mercury-in-silastic strain gauges. Blood flow in the cannulated arm increased significantly during the first ANP infusion; by 52 +/- 15% before placebo (P less than 0.05), and by 41 +/- 8% before enalaprilat (P less than 0.005). This increase was similar with the second ANP infusion during co-infusion of either placebo (40 +/- 10%) or enalaprilat (45 +/- 11%). Enalaprilat did not affect the half-life of vasodilatation produced by ANP (t1/2 = 5 min). These studies in healthy subjects demonstrate no effect of local ACE inhibition on resting blood flow, or on the vasodilatation produced by ANP in the human forearm, and provide no evidence of a role of ACE in the metabolism of ANP in this vascular bed.
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PMID:The effect of local angiotensin converting enzyme inhibition on the action of atrial natriuretic peptide in the human forearm. 254 49

The study was designed to compare the efficacy of captopril and enalapril, both orally active inhibitors of angiotensin converting enzyme, in the treatment of primary hypertension when administered in a single daily dose. After placebo washout for two weeks, 20 hypertensive patients (I-II class, according to WHO), were admitted to active treatment, in a randomized sequence, with captopril (50 mg) and enalapril (20 mg) once a day in the morning (8 a.m.). Supine and erect blood pressure and heart rate were measured weekly, 24 hours after drug administration by using a mercury standard sphygmomanometer. In all patients ambulatory noninvasive blood pressure monitoring was performed after 4 weeks of treatment. The data confirmed the efficacy of both drugs in lowering blood pressure. However, while the antihypertensive effect of enalapril was prolonged throughout 24 hours, captopril was effective only for about 22 hours, a period longer than previously suggested on the basis of serum ACE inhibition, but not sufficient to cover the whole day. Therefore, if captopril therapy has to be used in a single daily dose an attempt should be made using an increased dosage or by employing the drug in some retarded pharmaceutical form. The need to prolong the antihypertensive effect of captopril to 24 hours is based on the clinical experience according to which the smaller the number of tablets to be taken the better the compliance. This is particularly true for cases of asymptomatic hypertension which nevertheless require lifelong therapy.
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PMID:[Comparison of the efficacy of captopril and enalapril in single doses in the treatment of arterial hypertension. Evaluation by means of non-invasive ambulatory monitoring]. 255 65

Pharmacotherapy of hypertension in the aged does not differ qualitatively but only quantitatively from that in use for younger patients. Adjusted, usually lower doses of diuretics, beta-blocking agents, ACE-inhibitors and calcium-channel blockers are the basic drugs. Individual aging processes and concomitant diseases determine the choice of drugs in the elderly (individualized therapy). All substances are initially prescribed at very low dose. The increasing infirmity of the aged often associated with tiredness, dyspnea and dizziness even without treatment requires careful instruction of the patient about effects and side effects of the prescribed medication. The old WHO-guidelines (systolic BP greater than or equal to 160, diastolic BP greater than or equal to 95 mm mercury) should be maintained for diagnosis and treatment of hypertension. However antihypertensive therapy in patients over 80 years of age and in those with marginally elevated diastolic or solely elevated systolic pressure is controversial today.
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PMID:[Hypertension and old age]. 268 25

ACE inhibitors are not available in India. Response to captopril in comparison with M-dopa was therefore seen in Indian hypertensive patients. A double blind randomized non-crossover study was carried out on 39 adult patients of either sex suffering from essential hypertension. Twenty-five patients included were resistant to earlier drug therapy. The remaining 14 were freshly detected hypertensive patients. Patients received either 150 mg/day captopril (Aceten) or 750 mg/day M-dopa in 3 equally divided doses every day for 30 days. The mean systolic and diastolic blood pressure in captopril (Aceten) group before starting drug therapy was 171 +/- 4.11 (mean +/- SE) and 111 +/- 0.22, respectively. At the end of therapy the systolic blood pressure was 132 +/- 1.86 and diastolic blood pressure was 84 +/- 1.36 mm of mercury. This fall in the blood pressure within the group was statistically highly significant (p less than 0.001). Similarly patients on M-dopa produced statistically highly significant fall in blood pressure (p less than 0.001) at the end of 4 weeks therapy. Initial systolic and diastolic blood pressure in both groups were comparable and, at the end of 2 and 4 weeks therapy, patients on captopril (Aceten) showed greater fall in both systolic (p less than 0.001) and diastolic (p less than 0.005) blood pressure than patients on M-dopa. None of the patients in the trial demonstrated clinically significant changes in the biochemical parameters. Six of nineteen patients on methyl dopa had side effects which are well known to this drug. None in the captopril showed any side effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical trial of captopril (Aceten) in Indian patients with essential hypertension. 353 Oct 33

The new angiotensin converting enzyme inhibitor enalapril (MK-421), was given in a single daily dose of 20 mg to 53 patients with uncomplicated essential hypertension. Its effects were compared with those of a placebo given to 47 patients on a double-blind randomized basis. The blood pressure was measured in all patients by a physician, using a mercury sphygmomanometer, and by an automatic device in the absence of the physician. After 15 days of treatment, enalapril induced a significant reduction in systolic blood pressure (161.4 +/- 13 versus 145.1 +/- 15, p less than 0.001) and in diastolic blood pressure (103.3 +/- 6 versus 92.9 +/- 8, p less than 0.001) measured by the physician. The magnitude of the fall in blood pressure was identical after 30 days of active treatment. The reduction in blood pressure induced by enalapril was similarly detected by both methods of measurement, despite the fact that blood pressure values were higher when measured by the physician. A placebo effect was observed with the physician's values that was not present with the automatically recorded values. A very significant correlation between blood pressure values obtained by these two methods was observed. However, among nine of 53 patients treated with enalapril, a difference in the decrease of blood pressure of 10 mm Hg or more was noted between the two methods of measurement. The decrease in blood pressure occurred with no change noted in the pulse rate or orthostatic hypotension. Plasma renin activity increased after treatment. No changes were observed in creatinine clearance and plasma electrolyte levels.
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PMID:Antihypertensive effect of enalapril as first-step treatment of mild and moderate uncomplicated essential hypertension. Evaluation by two methods of blood pressure measurement. 608 55

The experiments referred to in this article point to the fact that relatively low concentrations of Hg2+ (5-10 mM) produce damage to the internal mitochondrial membrane. This damage results in the formation of ionic channels that allow the spontaneous effusion of Ca+2 from the matrix. Together with this, the formation of channels produce the balance of the chemo-osmotic gradient, resulting in the overcoming of the transmembrane potential and the uncoupling of oxidative phosphorylation. The experiments carried out in vivo, point to the fact mercury produces acute tubular necrosis of kidney tissue. These toxic effects produced by Hg2+ in vitro with the addition of 15 microM of the inhibition of the angiotensin converting enzyme, captopril. In vivo experiments show that intraperitoneal infection of captopril (40 mg/kg) completely protects from mitochondrial dysfunction produced by mercurial intoxication.
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PMID:[Captopril protection from the nephrotoxic effects of mercury]. 765 76

The aim of the present study was to examine the relationships between ambulatory blood pressure (ABPM) and urinary albumin excretion (UAE) in diabetic (non-insulin dependent [NIDDM] and insulin-dependent [IDDM]) hypertensives at baseline and after treatment by an angiotensin converting enzyme (ACE) inhibitor. After a 3-week placebo period, patients were treated for 16 weeks with trandolapril, 2 to 4 mg/day. The UAE and blood pressure (mercury sphygmomanometer and 24-h ABPM) were measured at baseline and repeated on trandolapril. Predictive factors of abnormal UAE (24-h UAE > or = 30 mg) were determined using univariate and multivariate analysis (logistic regression). Predictors of UAE decrease were also searched. One hundred seventy-one patients entered the analysis. Baseline office BP was 164+/-14 / 97+/-6 mm Hg and 24-h BP was 142+/-17 / 83+/-10 mm Hg. Seventy-four patients (43%) had UAE > or = 30 mg. Independent risk factors for abnormal UAE were nighttime diastolic BP (odds ratio [OR] = 4.1, confidence interval [CI] = 2.0 to 8.6, P = .0001), diabetes duration (OR = 2.4, CI = 1.1 to 5.0, P = .025), and presence of retinopathy (OR = 3.2, CI = 1.0 to 10.0, P = .047). Conversely, office BP level was not significantly related to UAE. On treatment, office BP levels decreased to 143+/-13 / 82+/-8 mm Hg (P < .0001) and 24-h BP levels to 134+/-17 / 78+/-9 mm Hg (P < .0001). In the abnormal UAE group, UAE significantly decreased from 76 to 50 mg/day (P = .006). After treatment, independent predictive factors of abnormal UAE were: on-drug fasting plasma glucose (OR = 3.5, CI = 1.7 to 7.4, P = .0009) and on-drug nighttime diastolic BP (OR = 3.5, CI = 1.7 to 7.4, P = .001). The only predictor of UAE decrease was a 24-h systolic BP decrease (OR = 2.3, CI = 1.3 to 4.3, P = .007). We conclude that in diabetic hypertensives with abnormal UAE, trandolapril exhibited a sustained 24-h antihypertensive effect and provided a consistent reduction of microalbuminuria. This study confirmed the superiority of ABPM over clinical BP to predict target organ damage.
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PMID:Ambulatory blood pressure and urinary albumin excretion in diabetic (non-insulin-dependent and insulin-dependent) hypertensive patients: relationships at baseline and after treatment by the angiotensin converting enzyme inhibitor trandolapril. 975 91

The aim of this study was to analyse the effect of the ACE-1, Trandolapril, alone or with Verapamil on blood pressure, albuminuria and metabolic profile in type 2 diabetic patients with hypertension and albuminuria. It was an open multicenter, consecutive and prospective study conducted in 281 patients. There was a four-week wash-out period of antihypertensive drugs, after which we carried out a measurement over a 24-h period of the urinary excretion of albumina (UEA). Blood pressure was recorded after at least 5 minutes of rest in the sitting position at 1 to 3 minute intervals with a mercury sphygmomanometer in good condition. Average BP was obtained from three consecutive readings. Within treatment changes were analysed using descriptive statistics and t-tests on the change from baseline. Analysis of variance, chi-square and Mc Nemar tests were also used. If after 8 weeks of treatment with Trandolapril 2 mg o.q.d. the patients were non-responders (mean blood pressure reduction of 5 mmHg or less) or their blood pressure remained uncontrolled (blood pressure > or = 140/90 mmHg), Verapamil 180 mg o.q.d. was added. Two hundred and thirty patients completed the 12 weeks study. Population included 157 (55.9%) males with an average of 61.7 +/- 9.2 years. Baseline measurements were systolic 165.4 +/- 14.6 and diastolic 94.8 +/- 8.5 mmHg blood pressures, fasting glucose 162.7 +/- 43.9 mg/dL, glycosylated hemoglobin (HbAlc) 6.8 +/- 1.2%, and albuminuria 520.9 +/- 602 mg/day. UEA fell significantly (p < 0.001) after treatment to 177.9 +/- 24.3 mg/day (CI 95%, 129.9 to 225.8). The percent reduction reached 29.6%. Albuminuria was lower than 30 mg/day in 47 patients. Blood pressure was completely controlled in 125 (54%) patients. Glucemia fell significantly (p < 0.001) to 153.2 +/- 42.7 mg/dL, and the HbAlc to 6.5 +/- 1.3% (p = 0.012). In summary, in those diabetic type 2 patients with arterial hypertension and proteinuria, Trandolapril alone or associated with Verapamil significant lowered albuminuria and blood pressure facilitated the control or their metabolic profile.
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PMID:[The effect of trandolapril, in monotherapy and associated with verapamil, on arterial pressure, albuminuria, and metabolic control in hypertensive patients with type 2 diabetes and albuminuria]. 1179 14

Elevated arterial pressure had long been surmised from the strength of the pulse. Its association with contracted kidneys and hypertrophied hearts was described by Richard Bright (1789-1858). Microscopic observations of the narrowed and obliterated vasculature initially observed in the kidneys of Bright's disease, and subsequently throughout the body, launched clinical research into hypertension. The description of these findings in the absence of symptoms of kidney disease led to the recognition of primary hypertension. Ultimately, the systematic recording of the blood pressure with a pneumatic cuff and mercury manometer established the significance of hypertension as a distinct disease entity. Subsequent experimental studies established the central role of the kidney in hypertension through the renin-angiotensin system and extracellular volume control. This finding provided the basis for the introduction of diuretics and angiotensin converting enzyme inhibitors, two of the most important and valuable antihypertertensive drugs now available. Thus, the study of kidney disease and function has played a pivotal role in the conceptual evolution of the understanding of hypertension as a disease, the identification of its mechanisms, and the development of clinically useful antihypertensive medications.
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PMID:On the central role of studies on the kidney in the recognition, conceptual evolution, and understanding of hypertension. 1521 90


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