TY - JOUR. T1 - Utility of the ACE Inhibitor Captopril in Mitigating Radiation-Associated Pulmonary Toxicity in Lung Cancer. AU - Small, William. AU - James, Jennifer L.. AU - Moore, Timothy D.. AU - Fintel, Dan J.. AU - Lutz, Stephen T.. AU - Movsas, Benjamin. AU - Suntharalingam, Mohan. AU - Garces, Yolanda I.. AU - Ivker, Robert. AU - Moulder, John. AU - Pugh, Stephanie. AU - Berk, Lawrence B.. PY - 2018/1/1. Y1 - 2018/1/1. N2 - Objectives: The primary objective of NRG Oncology Radiation Therapy Oncology Group 0123 was to test the ability of the angiotensin-converting enzyme inhibitor captopril to alter the incidence of pulmonary damage after radiation therapy for lung cancer; secondary objectives included analyzing pulmonary cytokine expression, quality of life, and the long-Term effects of captopril. Materials and Methods: Eligible patients included stage II-IIIB non-small cell lung cancer, stage I central non-small cell lung cancer, or limited-stage small cell. Patients who met eligibility ...
Objectives. This study attempted to evaluate whether neurohumoral activation at the time of hospital discharge in postinfarction patients helps to predict long-term prognosis and whether long-term therapy with the angiotensin-converting enzyme inhibitor captopril modifies this relation.. Background. Neurohumoral activation persists at the time of hospital discharge in a large number of postinfarction patients. The Survival and Ventricular Enlargement (SAVE) study demonstrated that the angiotensin-converting enzyme inhibitor captopril improves survival and decreases the development of severe heart failure in patients with left ventricular dysfunction (left ventricular ejection fraction ≤40%) but no overt postinfarction heart failure.. Methods. In 534 patients in the SAVE study, plasma neurohormone levels were measured a mean of 12 days after infarction. Patients were then randomized to receive captopril or placebo and were followed up for a mean (±SD) of 38 ± 6 months (range 24 to 55). The ...
The most remarkable observations of the study were related to the comparative effects of poststroke losartan versus captopril treatment. After 31 days of losartan treatment, the MCAs of SHRsp regained the ability to constrict in response to pressure and NOS inhibition. Such treatment also restored vasodilator function in response to bradykinin, established prestroke oscillatory characteristics, and enhanced vasodilation in response to A23187. Captopril treatment did not duplicate these effects. A short (7 day) duration of captopril treatment allowed the MCAs of SHRsp to temporarily regain these functions; however, after 18 days of treatment, these cerebrovascular functions deteriorated. After 31 to 37 days of captopril treatment, the characteristics of PDC, constriction in response to NOS inhibition, and bradykinin vasodilation were not different from those observed in the MCAs of SHRsp at the time of stroke. The differences in the action of losartan versus captopril cannot be explained on the ...
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TY - JOUR. T1 - Hemodynamic and clinical significance of the pulmonary vascular response to long-term captopril therapy in patients with severe chronic heart failure. AU - Packer, M.. AU - Lee, W. H.. AU - Medina, N.. AU - Yushak, M.. PY - 1985/1/1. Y1 - 1985/1/1. N2 - Exercise capacity in patients with left heart failure is closely related to the performance of the right ventricle and the pulmonary circulation. To determine the significance of changes in pulmonary resistance during longterm vasodilator therapy, hemodynamic studies were performed before and after 1 to 3 months of treatment with captopril in 75 patients with severe chronic left heart failure. Patients were grouped according to the relative changes in pulmonary and systemic resistances during long-term therapy: patients in Group I (n = 24) showed greater decreases in pulmonary arteriolar resistance (PAR) than in systemic vascular resistance (SVR) (% Δ PAR/% Δ SVR,1.0), whereas patients in Group II showed predominant systemic ...
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Nine patients with uncomplicated essential hypertension received, according to a randomized sequence, captopril (25 mg three times daily), nifedipine (10 mg three times daily), and both drugs for 1 week, with each treatment period separated by a 1-week interval during which a placebo was given. Captopril significantly reduced blood pressure and plasma aldosterone, increased plasma renin activity (PRA), and did not change heart rate. Nifedipine exerted a similar effect on blood pressure and PRA, but it increased heart rate and did not change aldosterone. Captopril plus nifedipine further reduced blood pressure and increased PRA, did not change heart rate, and reduced aldosterone to values similar to those after captopril alone. The hypotensive effect of captopril was highly predictable by basal PRA values, and that of nifedipine by age, while PRA increments induced by captopril were unrelated to those induced by nifedipine. These data indicate that: 1) captopril and nifedipine exert an additive ...
TY - JOUR. T1 - The angiotensin converting enzyme inhibitor captopril protects nigrostriatal dopamine neurons in animal models of parkinsonism. AU - Sonsalla, Patricia K.. AU - Coleman, Christal. AU - Wong, Lai Yoong. AU - Harris, Suzan L.. AU - Richardson, Jason R.. AU - Gadad, Bharathi S.. AU - Li, Wenhao. AU - German, Dwight C.. PY - 2013/12. Y1 - 2013/12. N2 - Parkinsons disease (PD) is a progressive neurodegenerative disorder characterized by a prominent loss of nigrostriatal dopamine (DA) neurons with an accompanying neuroinflammation. The peptide angiotensin II (AngII) plays a role in oxidative-stress induced disorders and is thought to mediate its detrimental actions via activation of AngII AT1 receptors. The brain renin-angiotensin system is implicated in neurodegenerative disorders including PD. Blockade of the angiotensin converting enzyme or AT1 receptors provides protection in acute animal models of parkinsonism. We demonstrate here that treatment of mice with the angiotensin ...
The captopril challenge test (CCT) is a non-invasive medical test that measures the change in renin plasma-levels in response to administration of captopril, an angiotensin converting enzyme inhibitor. It is used to assist in the diagnosis of renal artery stenosis. It is not generally considered a useful test for children, and more suitable options are available for adult cases. Plasma concentration of renin is measured prior to and following the administration of captopril. The CCT is considered positive if the renin levels increase substantially or the baseline renin level is abnormally high. An abnormal captopril test is indicative of the presence of renovascular disease. CCT in adults is known to have high sensitivity, but a low specificity. Subtraction angiography is considered a more suitable test for renal artery stenosis in adults. Contrast with captopril suppression test used to diagnose primary aldosteronism Gauthier B, Trachtman H, Frank R, Pillari G. Inadequacy of captopril challenge ...
TY - JOUR. T1 - Effect of Captopril on Mortality and Morbidity in Patients with Left Ventricular Dysfunction after Myocardial Infarction. T2 - Results of the Survival and Ventricular Enlargement Trial. AU - Pfeffer, Marc A.. AU - Braunwald, Eugene. AU - Moyé, Lemuel A.. AU - Basta, Lofty. AU - Brown, Edward J.. AU - Cuddy, Thomas E.. AU - Davis, Barry R.. AU - Geltman, Edward M.. AU - Goldman, Steven. AU - Flaker, Greg C.. AU - Klein, Marc. AU - Lamas, Gervasio A.. AU - Packer, Milton. AU - Rouleau, Jean L.. AU - Rutherford, John. AU - Rouleau, Jean L.. AU - Wertheimer, John H.. AU - Hawkins, C. Morton. PY - 1992/9/3. Y1 - 1992/9/3. N2 - Left ventricular dilatation and dysfunction after myocardial infarction are major predictors of death. In experimental and clinical studies, long-term therapy with the angiotensin-converting-enzyme inhibitor captopril attenuated ventricular dilatation and remodeling. We investigated whether captopril could reduce morbidity and mortality in patients with left ...
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Numerous studies have shown favorable effects on parameters of LV remodeling for drugs that improve clinical outcomes in patients with decreased LVEF and LV dilation, notably angiotensin-converting enzyme inhibitors, beta-blockers, and angiotensin receptor blockers (14,15,18,57,63-69). Conversely, agents with neutral or adverse effects on remodeling, relative to a comparator, have often been found to be associated with neutral or adverse effects on clinical outcomes. Examples include omapatrilat (70,71) and ibopamine (72,73). In a head-to-head comparison of the angiotensin-converting enzyme inhibitor captopril, 150 mg daily, with the angiotensin receptor blocker losartan, 50 mg daily, we found a trend favoring captopril in the 1-year change in LV volumes (18), an effect that presaged the mortality findings in ELITE (Early Versus Late Intervention Trial With Estradiol) II (74). Yu et al. (75) showed that a decrease in LV ESV of ≥10% after cardiac resynchronization therapy predicted decreased ...
Pulmonary vascular remodeling is one of the typical responses to chronic alveolar hypoxia in the rat model of pulmonary hypertension (PH). Neither the etiology nor the structural and functional consequences of this remodeling are well understood. It is known that chronic treatment with ACE inhibitors results in a reduction of lung perfusion pressures and vascular changes in hypoxic PH, but the effect of treatment with ACE inhibitors on arterial tree morphology and mechanical properties of the artery walls in the intact lung have not been examined. In addition to using standard hemodynamic analysis, we approach this problem with x-ray micro-CT imaging and measure the distensibility of pulmonary arteries (approximate range of 50 - 2000 um diameter) in rat lungs. We examine consequences of chronic hypoxic exposure (10% O2) with and without Captopril treatment in FH, SD and BN rats. The FH rat strain is known to possess a genetic susceptibility to PH whereas the BN strain is resistant to PH. An example of
Acute reversible renal failure may complicate therapy with Captopril in patients with bilateral renal-artery stenoses or renal-artery stenosis in a solitary kidney (1-6). The concomitant use of diuretic agents in many of the reported cases of captopril-induced renal insufficiency has led to speculation that diuretic therapy or sodium depletion may contribute to the decrement in glomerular filtration rate mediated by angiotensin-converting enzyme inhibitors in the presence of a fixed reduction in renal perfusion pressure (1, 6). To determine the influence of sodium balance on captopril-induced renal insufficiency, the renal hemodynamic effects of Captopril were studied prospectively in a patient with ...
The interaction of the renin-angiotensin system and the sympathetic nervous system in patients with congestive heart failure is not well understood. We tested the hypothesis that angiotensin-converting enzyme inhibitors can resensitize the beta-adrenergic receptor system. Guinea pigs were given captopril, isoproterenol, or both for 2 weeks. At death, cardiac sarcolemmal and light vesicle fractions and intact mononuclear leukocytes were prepared. Captopril treatment led to an up-regulation of cardiac beta 1- but not mononuclear leukocyte beta 2-adrenergic receptors and an increase in isoproterenol-stimulated adenylate cyclase activity in the heart. Animals treated with isoproterenol developed cardiac hypertrophy, had increased plasma norepinephrine levels, and had a decreased number and responsiveness of both cardiac and mononuclear leukocyte beta-adrenergic receptors. Concomitant treatment with captopril attenuated alterations of heart weight, plasma norepinephrine levels, and cardiac ...
Increased generation of reactive oxygen species (ROS) is a significant pathological feature in the brains of patients with Alzheimers disease (AD). Experimental evidence indicates that inhibition of brain ROS could be beneficial in slowing the neurodegenerative process triggered by amyloid-beta (Abeta) aggregates. The angiotensin II AT1 receptor is a significant source of brain ROS, and AD patients have an increased brain angiotensin-converting enzyme (ACE) level, which could account for an excessive angiotensin-dependent AT1-induced ROS generation. Therefore, we analyzed the impact of ACE inhibition on signs of neurodegeneration of aged Tg2576 mice as a transgenic animal model of AD. Whole genome microarray gene expression profiling and biochemical analyses demonstrated that the centrally active ACE inhibitor captopril normalized the excessive hippocampal ACE activity of AD mice. Concomitantly, the development of signs of neurodegeneration was retarded by six months of captopril treatment. The ...
Generic Name: captopril (KAP-toe-pril) Brand Name: Generic only. No brands available. Captopril can cause injury and possibly death to a fetus if used during pregnancy. Talk with your doctor right away if you suspect that you are pregnant. If you are planning to become pregnant, talk with your doctor ...
The captopril suppression test (CST) is a non-invasive medical test that measures plasma levels of aldosterone. Aldosterone production is suppressed by captopril through the renin-angiotensin-aldosterone system. CST results are used to assist in the diagnososis of primary aldosteronism (Conn Syndrome). Contrast with captopril challenge test used to diagnose renal artery stenosis Agharazii M, Douville P, Grose JH, Lebel M (June 2001). "Captopril suppression versus salt loading in confirming primary aldosteronism". Hypertension. 37 (6): 1440-3. doi:10.1161/01.hyp.37.6.1440. PMID 11408392 ...
نبذة مختصرة. Heart failure with preserved ejection fraction (HFpEF), a prevalent form of heart failure, is frequently accompanied by the metabolic syndrome and kidney disease. Because current treatment options of HFpEF are limited, evaluation of therapies in experimental models of HFpEF with the metabolic syndrome and kidney disease is needed. In this study, we evaluated the effects of captopril, furosemide, and their combination in aged, obese ZSF1 rats, an animal model of HFpEF with the metabolic syndrome and chronic kidney disease as comorbidities. Captopril (100 mg/kg), furosemide (50 mg/kg), or their combination was administered orally to obese ZSF1 rats aged 20 to 44 weeks. Untreated ZSF1 rats served as controls. After 24 weeks of treatment, captopril significantly lowered systemic blood pressure and attenuated HFpEF as evidenced by significantly reduced left ventricular end diastolic pressures (10.5 ± 1.4 vs. 4.9 ± 1.3 mm Hg in Control vs. Captopril, respectively) and ...
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The medium Benadryl dosage for dogs is one mgpound. Acquired Allergic reactions can also be affected, so use your doctor judgment to determine if the dogs allergies warrant emergency care. Never use special-release capsules for dogs, as does are absorbed differently in formulas molecular del captopril than in injuries and may feel your dogs formula molecular del captopril. They may also break crush when chewed and deliver too much worse at one time, putting your dog at december of an overdose. If you harm to use a liquid Benadryl. How good is Benadryl for headaches. Also, what is the recommended Benadryl dosage for dogs. Molecular Formula: C9H15NO3S. Formula Molecular. El captopril es un inhibidor de la enzima conversora de la. Su biodisponibilidad es del 60 - 75%. La fórmula iupac es la dci o denominación común internacional y esa es captopril, ahora si lo que preguntás es la denominacíon química me.. ...
The effects of 6 weeks of treatment with captopril on the renal hemodynamics of 16 patients with treatment-resistant renal hypertension (six had diabetic nephropathy, seven had other renal parenchymatous disease, and three had renovascular disease) were studied. Significant changes in glomerular filtration rate, filtration fraction, plasma renin activity, urinary aldosterone, and mean blood pressure were noted in the patients with renal parenchymatous disease, but not in those with diabetic nephropathy. Renal blood flow remained unchanged in all patients. Captopril was well tolerated. ...
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Generic Name: captopril (KAP-toe-pril) Brand Name: Generic only. No brands available. Captopril can cause injury and possibly death to a fetus if used during pregnancy. Talk with your doctor right away if you suspect that you are pregnant. If you are planning to become pregnant, talk with your doctor ...
BACKGROUND: Although oral administration of captopril, an angiotensin-converting enzyme inhibitor, is effective for the treatment of congestive heart failure (CHF), the effect of its intravenous (iv) administration is not well known. METHODS AND RESULTS: Ten patients (age range 48-72 years), with CHF belonging to the second and third NYHA class, were given an iv bolus of 25 mg of captopril. Before and 30 minutes after the infusion of captopril, a number of parameters of the left ventricular function were evaluated by echocardiography IREX 3 M-B Mode. Eight patients showed a significant improvement of left ventricular performance indices. In fact, the ejection fraction (13.8%, p , 0.05), the cardiac output (24%, p , 0.001), the circumferential shortness fraction (29.9%, p , 0.05), and the fraction shortening (16.0%, p , 0.005) increased significantly, whereas the end-systolic diameter (21%, p , 0.001), the endsystolic stress (23.8%, p , 0.01) and the left ventricle ejection time (4.8%, p , 0.05) ...
It is important to consider secondary causes of hypertension (eg, renovascular hypertension) that may have precipitated the crisis. A single dose captopril (Capoten) challenge test may be performed, particularly in patients who have not received previous medical therapy for hypertension. Baseline plasma renin activity is measured and the patient is given 25 to 50 mg of captopril; measurement is repeated 60 minutes later. Test sensitivity is excellent but specificity is poor. Thus, further testing (eg, renal arterial Doppler ultrasonography, renal magnetic resonance angiography, contrast angiography) may be necessary to confirm diagnosis. Before initiating therapy, metanephrine levels can be measured by performing spot urine test to rule out the presence of pheochromocytoma. Plasma aldosterone and renin levels should be tested to rule out primary hyperaldosteronism in patients with significant hypokalemia who are not taking diuretics at the time of presentation.. Captopril Screening ...
Resumo: Neste trabalho os fármacos anti-hipertensivos captopril e hidroclorotiazida foram alvo de estudo por duas abordagens: (a) analítica, com o objetivo de desenvolver e validar método por CLAE-DAD para sua determinação e de seus compostos relacionados simultaneamente em comprimidos e (b) do ponto de vista do controle de qualidade com o objetivo de avaliar a equivalência farmacêutica e perfil de dissolução dos medicamentos disponíveis comercialmente que os contenham separadamente ou associados. Foi desenvolvido e validado um método rápido e econômico utilizando CLAE-DAD para quantificação de captopril (CAP), hidroclorotiazida (HCTZ) e seus principais compostos relacionados: dissulfeto de captopril (CAD), clorotiazida (CTZ) e benzotiadiazina (BTDZ). O método foi desenvolvido e validado através de um sistema cromatográfico composto por uma coluna Agilent Zorbax Eclipse XDB-Phenyl 5 ?m, 4,6 x150 mm mantida a 40°C, utilizando como fase móvel (A) ácido fosfórico 0,067% (pH ...
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Captopril can be used alone in treating high blood pressure. Its blood pressure lowering effect can be further enhanced by the addition of a diuretic (water pill) medication. Capozide is an example of a medication that combines the effect of Captopril with a diuretic (water pill). By reducing resistance in the arteries, Captopril can be useful in the treatment of congestive heart failure. In treating heart failure, Captopril usually supplements conventional treatment, including a diuretic and digoxin (Lanoxin). After a heart attack, Captopril has been found to be effective in improving functioning of the damaged heart. It is also used to treat kidney disease associated with diabetes ...
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Several trials have shown that converting enzyme inhibitors (CEI) reduce mortality in patients with heart failure. More recent studies have tested CEIs after acute MI. In the CONSENSUS II trial (1), enalapril was begun intravenously and a nonsignificant higher mortality rate was found, whereas investigators of the more recent GISSI-3 (2) found that oral lisinopril significantly reduced 6-week mortality. Now, the ISIS-4 investigators have also found a significant lower mortality rate at 5 weeks with the use of oral captopril. Hypotension was more common among patients treated with CEIs in each trial. The findings suggest that CEIs begun soon after onset of MI reduce short-term mortality, although care is necessary in starting therapy, especially in patients with systolic blood pressure , 100 mm Hg. Patients at higher risk may have greater mortality reductions from CEI therapy because of their lower ejection fractions, especially patients with either anterior MI or previous MI. The ISIS-4 ...
Captopril, is an angiotensin-converting enzyme inhibitor used for the treatment of hypertension and some types of congestive heart failure.
Captopril is an ACE inhibitor. ACE stands for Angiotensin Converting Enzyme. Captopril is used to treat high blood pressure (hypertension), congestive heart failure, kidney problems caused by diabetes, and to improve survival after a heart attack. ...
Administration of captopril results in a reduction of peripheral arterial resistance in hypertensive patients with either no change, or an increase in cardiac output. There is an increase in renal blood flow following administration of captopril and glomerular filtration rate is usually unchanged.. Reductions of blood pressure are usually maximal 60 to 90 minutes after oral administration of an individual dose of captopril. The duration of effect is dose related. The reduction in blood pressure may be progressive, so to achieve maximal therapeutic effects, several weeks of therapy may be required. The blood pressure lowering effects of captopril and thiazide-type diuretics are additive. In contrast, captopril and beta-blockers have a less than additive effect.. Blood pressure is lowered to about the same extent in both standing and supine positions. Orthostatic effects and tachycardia are infrequent but may occur in volume-depleted patients. Abrupt withdrawal of captopril has not been associated ...
Lactacystin is a proteasome inhibitor that interferes with several factors involved in heart remodelling. The aim of this study was to investigate whether the chronic administration of lactacystin induces hypertension and heart remodelling and whether these changes can be modified by captopril or melatonin. In addition, the lactacystin-model was compared with NG-nitro-l-arginine-methyl ester (L-NAME)- and continuous light-induced hypertension. Six groups of three-month-old male Wistar rats (11 per group) were treated for six weeks as follows: control (vehicle), L-NAME (40 mg/kg/day), continuous light (24 h/day), lactacystin (5 mg/kg/day) alone, and lactacystin with captopril (100 mg/kg/day), or melatonin (10 mg/kg/day). Lactacystin treatment increased systolic blood pressure (SBP) and induced fibrosis of the left ventricle (LV), as observed in L-NAME-hypertension and continuous light-hypertension. LV weight and the cross-sectional area of the aorta were increased only in L-NAME-induced hypertension. The
Captopril is an ACE inhibitor. ACE stands for angiotensin converting enzyme. Captopril is used to treat high blood pressure (hypertension), congestive heart
Side effects may occur with captopril, but gradual weight gain doesnt appear to be one of them. This eMedTV page explains why the link between captopril and weight gain is unlikely, but also offers weight-loss tips for those who develop the problem.
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This study is a sequel to a previous study by McGrowder et al. [9] which found that SNAP-treated dogs displayed postprandial hyperglycaemia. Captopril was used as the control drug based on results from a study conducted by Winocour et al. [10] which found that low-dose therapy had no significant effect on blood glucose control in hypertensive insulin-treated diabetic individuals and that it lowers blood pressure by a mechanism which is different from SNAP. The study by McGrowder et al. [9] also reported that SNAP at 20 mg/kg caused significant reduction of the haemodynamic parameter, mean arterial pressure and a significant increase in heart rate via the release of nitric oxide. Captopril at a dose of 20 mg/kg had less of an effect on both mean arterial and heart rate. The mean arterial blood pressure-lowering effect of captopril (an angiotensin converting enzyme inhibitor) is related to a reduction in the peripheral arterial vascular resistance. The hypotensive response to captopril is ...
Renin (REN) expression is required to maintain blood pressure and electrolyte homeostasis. However, the mechanisms by which REN is transcriptionally regulated remain elusive. We reported a functional role for several nuclear receptors (NRs) on REN gene transcription. To identify other candidate NRs that regulate REN, we analyzed a publicly available microarray dataset (GUDMAP Developing Kidney ST1) to compare the expression pattern of REN and the 48 NRs across different kidney cell types. Our analysis revealed 14 NRs exhibiting a similar pattern as REN. We hypothesized that these NRs are co-regulated with REN and can regulate REN transcription. To test this hypothesis, we set up 2 cohorts of mice in which REN expression was either high or low compared to control mice and measured expression of REN and NRs in renal cortex by qPCR. The high-REN cohort was given the ACE inhibitor captopril (100g/kg/day) for 10 days, and the low-REN group was implanted subcutaneously with a deoxycorticosterone acetate
Mercurials are known to induce morphological and functional modifications in kidney mitochondria. In this work we studied in vitro and in vivo the protective effect of captopril on the deleterious effect of Hg(++)-induced nonspecific membrane permeability changes to Ca++ and membrane de-energization. In vivo the administration of captopril prevented the toxic effects of mercury poisoning on membrane permeability, oxidative phosphorylation and Ca++ homeostasis. Moreover, captopril preserves kidney tissue morphology from Hg(++)-induced damage. The protective effect of captopril is most likely related to the existence of a sulfhydryl group in the drug. ...
A study in the Journal of the American Pharmacists Association found that patients with type 2 diabetes taking captopril had a significantly higher risk of suffering from pulmonary adverse drug effects, compared with those taking other angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers. The researchers said the study highlights the importance of considering a medications adverse event profile and how they may affect pulmonary function in infections such as COVID-19.
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Captopril is an angiotensin converting enzyme (ACE) inhibitor prescribed for treating high blood pressure, heart failure, and for preventing kidney failure due to high blood pressure and diabetes. Learn about side effects, drug interactions, dosages, warnings, and more.
Various conditions can be treated with the medication captopril, which this eMedTV segment lists. This Web page also provides information on possible side effects and includes a link to a full-length article on this angiotensin II receptor blocker.
The authors deplore a recent incident that highlights the impact of the media and the pharmaceutical industry on the practice of medicine. The publication of a study comparing the changes in cholesterol levels and glucose metabolism of hypertensive patients treated with a diuretic and with an angiotensin converting enzyme inhibitor (captopril) was publicized by the pharmaceutical company that manufactures the latter drug. Alarmed by popular media reports that diuretics could raise heart attack risks, thousands of hypertensive patients being treated with diuretics contacted their physicians. A decrease in the number of new prescriptions for oral diuretics occurred in the months after the studys release. Citing data to show that diuretic therapy is still safe, effective, and relatively inexpensive in the management of hypertension, the authors call for physicians to take a stand against prescribing pressures generated by the media and by pharmaceutical industry promotion campaigns. (KIE abstract) ...
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