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)

The activity of the glycolytic enzymes and of the glucose-6-phosphate dehydrogenase (G-6-PDH) were compared with the content of noradrenaline in rat myocardium and the liver after the intraperitoneal injection of high doses of noradrenaline. It was shown that 24 hours after int noradrenaline injection which caused exhaustion of endogenous catecholamine supply, the lactate content and the activities of lactic dehydrogenase were increased in the myocardium; the activity of hexokinase and G-6-PDH in rat myocardium and the liver were also increased, whereas the glucokinase activity was decreased. In these experiments alterations of the enzyme activities were shown to be similar to the alterations in the dystrophic tissues in which the catecholamine content was sharply decreased. The role of the sympathetic nervous system and its mediators in the mechanism of the enzyme regulation of the energy metabolism in the myocardium and the liver is discussed.
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PMID:[Activity of energy metabolism related enzymes in the myocardium and liver following administration of large doses of noradrenaline]. 17 88

Since the therapeutic advances prolong survival of many patients suffering from cardiovascular pathology--the prevalence of chronic heart failure (CHF) had just doubled, being a common entity in a world whose individuals present a great increase in longevity. These considerations justify the renewed interest in this particular syndrome. Concepts, pathophysiology and compensatory mechanisms are briefly summarized, putting emphasis on the advantage of pharmacologically interrupt the vicious loop of the compensatory mechanisms, that could play a deleterious role in the syndrome. Neurohormonal responses and the "pivotal" role of angiotensine II in CHF pathology are also discussed, emphasizing the benefits of angiotensin converting enzyme inhibitors (ACEI) when treating patients presenting heart failure. Questions addressed to its prescription at an early stage, (classes II and III of NYHA--to prevent the progressive exhaustion of the failing heart) are also considered. When approaching the preventive measures in a wide perspective, primary, secondary and tertiary types of preventive options are described. ACEI use for the least advanced clinical stages of CHF (class II and III) would represent a tertiary type of CHF prevention.
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PMID:[Congestive heart insufficiency. Prophylactic aspects]. 269

Ten patients with congestive heart failure (CHF) (NYHA II-IV) on adjusted doses of digitalis and diuretics underwent a careful clinical assessment including an evaluation of exertion dyspnoea and the usual echocardiographic indices of cardiac performance. A cardiopulmonary exercise test with an increment of 20W every 3 minutes was prolonged until exhaustion. Systemic arterial pressure, ECG, VO2, VCO2 and VE were monitored throughout. Gas tensions, plasma catecholamines and lactate were measured in blood samples taken at the first and third minute of each exercise stage. The above measurements were carried out before and after 3 months of treatment with Captopril, 50 mg b.i.d. or t.i.d. A highly significant correlation between arterial lactate and plasma norepinephrine (NE) was observed in each patient during both exercise tests (r = 0.77 to 0.99; p less than 0.05 at least). Left ventricular end-diastolic dimensions were reduced by Captopril (from 69.9 +/- 1.7 to 65.2 +/- 1.4 mm, p less than 0.01) along with a concomitant increase in percent fractional shortening. Most of the patients were reclassified at a lower NYHA class and a significant decrease in dyspnoea score was observed. The exercise time was significantly increased (from 11.2 +/- 1.8 to 12.9 +/- 1.9 min; p less than 0.05), but the peak values of NE, arterial lactate and VO2 were not affected by the treatment. The predicted value of VE at a VCO2 of 1 L/min, regarded as an index of dyspnoea, was significantly decreased by Captopril (from 41.4 +/- 2.9 to 38.9 +/- 2.7 L/min; p less than 0.05). The positive effects of long-term treatment with Captopril on cardiac performance in CHF are confirmed. Sympathetic activity is linked to anaerobic muscular metabolism during exercise and seems to be independent of pharmacological ACE inhibition. The discrepancy between the exercise tolerance and the peak VO2 might be explained by a better utilization of the available energy.
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PMID:Sympathetic activation on effort in patients with chronic heart failure. Long term effects of captopril. 314 3

As a symptom of an underlying condition, cough is one of the most common reasons patients see physicians. To the majority, a cough means that 'something is wrong' and it causes exhaustion and/or self-consciousness. Patients find these reasons as well as effects on lifestyle, fear of cancer and/or AIDS or tuberculosis to be the most troublesome concerns for which they seek medical attention. The treatment of cough can be divided into two main categories: (a) therapy that controls, prevents or eliminates cough (i.e. antitussive); and (b) therapy that makes cough more effective (i.e. protussive). Antitussive therapy can be either specific or nonspecific. Definitive or specific antitussive therapy depends on determining the aetiology or operant pathophysiological mechanism, and then initiating specific treatment. Since the cause of chronic cough can almost always be determined, it is possible to prescribe specific therapy that can be almost uniformly successful. Non-specific antitussive therapy is directed at the symptom; it is indicated when definitive therapy cannot be given. Practically speaking, the efficacy of nonspecific therapy must be evaluated in double-blind, placebo-controlled, randomised studies of pathological cough in humans. Such studies have demonstrated the efficacy of dextromethorphan, codeine and ipratropium bromide aerosol in patients with chronic bronchitis. While the preferred treatment for patients with cough due to angiotensin converting enzyme (ACE) inhibitor therapy is withdrawal of the offending drugs, it may be possible to ameliorate the cough by adding nifedipine, sulindac or indomethacin to the treatment regimen. The efficacy of protussive therapy has not been well documented. Although hypertonic saline aerosol and erdosteine in patients with bronchitis, and amiloride aerosol in patients with cystic fibrosis have been shown to improve mucus clearance, their clinical utility has not been adequately studied.
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PMID:Appropriate use of antitussives and protussives. A practical review. 769 10

Hypertension in pregnancy remains a major cause of maternal and fetal morbidity and mortality. It is a late manifestation of a multifactorial, multisystem disease, initiated very early in pregnancy, the features of which suggest an inadequate maternal response to pregnancy. There is a genetic susceptibility to pre-eclampsia. Endothelial cell dysfunction in response to an unknown factor(s) may evoke some of the hormonal anomalies. In established severe disease there is volume contraction, reduced cardiac output, enhanced vascular reactivity, platelet exhaustion and disseminated intravascular coagulation in addition to the hypertension. Delivery is associated with resolution of the hypertension. Pharmacological treatment is most suitable for early-onset, severe disease when an attempt to delay delivery is indicated. Methyldopa or beta-blockers and/or vasodilators may be used. ACE inhibitors are contra-indicated. Low-dose aspirin may be useful in prophylaxis.
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PMID:Pre-eclampsia--the 'disease of theories'. 791 88

Six trained cyclists (high-fitness group) and six untrained individuals (low-fitness group), performed a 20-min cycle ergometer exercise test at 70% of maximum oxygen consumption (VO2max) followed by a 30-min rest period and then an incremental ride to exhaustion on two occasions, 1 week apart. Ninety minutes prior to exercise subjects consumed a drink containing either 22.2 g dibasic calcium phosphate (DCP; treatment) or calcium carbonate (placebo). Blood was drawn prior to drink ingestion, during submaximal exercise, during recovery and at exhaustion for determination of blood 2,3-DPG, blood ATP, plasma lactate, plasma phosphate, haemoglobin and haematocrit. Throughout exercise, cardiorespiratory variables [oxygen uptake (VO2), minute ventilation, (VE), respiratory exchange ratio, heart rate and oxygen pulse] were monitored, and ratings of perceived exertion obtained. Although there was a trend for the low-fitness group to have a higher plasma phosphate concentration prior to treatment ingestion, no treatment effects on plasma phosphate were noted at any sample time in either group. 2,3-DPG, VO2, oxygen pulse, VE, time to exhaustion and VO2max were significantly higher in the high-fitness group; however, no differences in these variables were observed as a result of phosphate ingestion. Plasma lactate was significantly lower in the high-fitness group during the submaximal exercise and the recovery period, but again phosphate ingestion had no effect. These results suggest that acute DCP supplementation is not effective as an ergogenic aid and that aerobic fitness level does not affect the response to phosphate supplementation.
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PMID:The effects of acute phosphate supplementation in subjects of different aerobic fitness levels. 882 Aug 90

Chronic hypoxia has been shown to increase plasma endothelin levels. The current study was undertaken to examine the effect of exercise-induced tissue hypoxia on plasma levels of endothelin-1 (ET-1) and its precursor big endothelin-1 (Big-ET-1). After approval by the local ethical committee an incremental dynamic exercise test was performed in 12 physically trained volunteers (aged 20 to 40 years), using an electrically braked bicycle ergometer. The protocol included a step-wise increase of the workload until a heart rate of 130/min was reached, followed by a maintenance period of 25 min, and a further step-wise increase until exhaustion. Blood was drawn before, at several time points during, and 5 min after termination of the study for determination of ET-1, Big-ET-1, plasma renin activity (PRA), angiotensin converting enzyme (ACE), norepinephrine, epinephrine, and lactate. Lactate levels at baseline were 14.5 +/- 1.6 mg/dL (mean +/- SEM), which increased to 76.5 +/- 4.8 mg/dL at the time of exhaustion (P < .01). Baseline values for ET-1 and Big-ET-1 were 0.264 +/- 0.061 and 0.637 +/- 0.130 fmol/ml, respectively, which remained essentially unaltered throughout the exercise test. PRA was 1.46 +/- 0.45 ng/mL/h before exercise and increased to 3.55 +/- 0.96 ng/mL/h at exhaustion (P < .001). Norepinephrine and epinephrine were also increased at exhaustion. The study demonstrates that exhaustive physical exercise with acute development of pronounced tissue hypoxia--in contrast to chronic hypoxia--does not influence the release of ET-1 or Big-ET-1 or the conversion of the precursor to the active compound. Unlike endothelin, circulating renin and the catecholamines were markedly stimulated by this maneuver.
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PMID:Exhaustive exercise-induced tissue hypoxia does not change endothelin and big endothelin plasma levels in normal volunteers. 971 98

The primary aim of the present study was to determine whether intramuscular triacylglycerol (IMTG) utilization contributed significantly to the increase in lipid oxidation during recovery from exercise, as determined from the muscle biopsy technique. In addition, we also examined the regulation of pyruvate dehydrogenase (PDHa) and changes in muscle acetyl units during an 18 h recovery period after glycogen-depleting exercise. Eight endurance-trained males completed an exhaustive bout of exercise (approximately 90 min) on a cycle ergometer followed by ingestion of carbohydrate (CHO)-rich meals (64-70 % of energy from carbohydrate) at 1, 4 and 7 h of recovery. Duplicate muscle biopsies were obtained at exhaustion, and 3, 6 and 18 h of recovery. Despite the large intake of CHO during recovery (491 +/- 28 g or 6.8 +/- 0.3 g kg-1), respiratory exchange ratio values of 0.77 to 0.84 indicated a greater reliance on lipid as an oxidative fuel. However, there was no net IMTG utilization during recovery. IMTG content at exhaustion was 23.5 +/- 3.5 mmol (kg dry wt)-1, and remained constant at 24.6 +/- 2.6, 25.7 +/- 2.8 and 28.4 +/- 3.0 mmol (kg dry wt)-1 after 3, 6 and 18 h of recovery. Muscle glycogen increased significantly from 37 +/- 11 mmol (kg dry wt)-1 at exhaustion, to 165 +/- 13, 250 +/- 18, and 424 +/- 22 mmol (kg dry wt)-1 at 3, 6 and 18 h of recovery, respectively. PDHa was reduced at 6 and 18 h when compared to exhaustion, but did not change during the recovery period. Acetyl-CoA, acetylcarnitine and pyruvate contents declined significantly after 3 h of recovery compared to exhaustion, and thereafter remained unchanged. We conclude that IMTG has a negligible role in contributing to the enhanced fat oxidation during recovery from exhaustive exercise. Despite the elevation of glucose and insulin following high-CHO meals during recovery, CHO oxidation and PDH activation were decreased, supporting the hypothesis that glycogen resynthesis is of high metabolic priority. Plasma fatty acids, very low density lipoprotein triacylglycerols, as well as intramuscular acetylcarnitine stores are likely to be important fuel sources for aerobic energy, particularly during the first few hours of recovery.
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PMID:Skeletal muscle fat and carbohydrate metabolism during recovery from glycogen-depleting exercise in humans. 1265 14

An important explanatory theory for the mechanism of postexercise proteinuria is that angiotensin II could be inhibited by angiotensin converting enzyme inhibitors. Because of the kininase effect of the angiotensin converting enzyme, it is unclear whether the kallikrein-kinin system contributes to the effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. The aim of this study was to evaluate any possible involvement of the kallikrein-kinin system in the therapeutic effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. We evaluated urinary protein levels in exhausted rats receiving an angiotensin converting enzyme inhibitor (enalapril) or an angiotensin II type I receptor antagonist (losartan). Enalapril (30 mg/kg/day, two days) or losartan (20 mg/kg/day, two days) were given to animals using an intragastric catheter. Urinary protein levels increased (41 %) in rats which were exhausted via treadmill running (p < 0.05). In animals that received drug treatment (enalapril or losartan), but did not exercise to exhaustion, urinary protein levels were not different from the control group. Urinary protein levels were found to be significantly lower (p < 0.05) in animals which performed acute exhaustive exercise after enalapril or losartan administration, compared to rats which were exhausted without drug administration. Inhibition of postexercise proteinuria by either enalapril or losartan suggested that angiotensin II plays an important role in postexercise proteinuria, however, it appears the kallikrein-kinin system is not involved in angiotensin converting enzyme inhibitors effect.
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PMID:Angiotensin II inhibition attenuates postexercise proteinuria in rats. 1623 14

In this study of effects of simulated altitude exposure on sea-level performance, 10 competitive runners slept in a hypoxic environment achieved with tents for 9.8+/-1.3 h.d(-1) (mean+/-standard deviation) for 24 days-30 days at 2500-3500 m (PIO2=117-103 mmHg) above sea level. The altitude group and a control group of 10 runners performed usual training (PIO2=149 mmHg). At approximately 4-wk intervals before and after exposure both groups performed an incremental test for lactate threshold. The altitude group performed an additional test, a treadmill run to exhaustion lasting approximately 5 min. One week following exposure lactate threshold speed of the altitude group relative to the control group increased by 1.2% (90% likely limits +/-3.1%), but the effect became slightly negative after controlling for baseline differences in running speed between the groups. A 16% increase in time to exhaustion was observed in the altitude group, equivalent to a 1.9% (+/-1.4%) increase in speed in a time trial. Change in performance had an unclear relationship to total altitude exposure, genotype for angiotensin converting enzyme, and change in haemoglobin concentration. Our findings are consistent with little or no effect of use of altitude tents on sea-level performance.
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PMID:Sea-level performance in runners using altitude tents: a field study. 1660 74


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