Angiotensin-Converting Enzyme Inhibitors: A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.Drug Labeling: Use of written, printed, or graphic materials upon or accompanying a drug container or wrapper. It includes contents, indications, effects, dosages, routes, methods, frequency and duration of administration, warnings, hazards, contraindications, side effects, precautions, and other relevant information.Peptidyl-Dipeptidase A: A peptidyl-dipeptidase that catalyzes the release of a C-terminal dipeptide, -Xaa-*-Xbb-Xcc, when neither Xaa nor Xbb is Pro. It is a Cl(-)-dependent, zinc glycoprotein that is generally membrane-bound and active at neutral pH. It may also have endopeptidase activity on some substrates. (From Enzyme Nomenclature, 1992) EC 3.4.15.1.Drug Repositioning: The deliberate and methodical practice of finding new applications for existing drugs.Product Labeling: Use of written, printed, or graphic materials upon or accompanying a product or its container or wrapper. It includes purpose, effect, description, directions, hazards, warnings, and other relevant information.Enalapril: An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.Captopril: A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.United States Food and Drug Administration: An agency of the PUBLIC HEALTH SERVICE concerned with the overall planning, promoting, and administering of programs pertaining to maintaining standards of quality of foods, drugs, therapeutic devices, etc.Lisinopril: One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.Prescription Drugs: Drugs that cannot be sold legally without a prescription.Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.User-Computer Interface: The portion of an interactive computer program that issues messages to and receives commands from a user.Computer Graphics: The process of pictorial communication, between human and computers, in which the computer input and output have the form of charts, drawings, or other appropriate pictorial representation.Software: Sequential operating programs and data which instruct the functioning of a digital computer.Programming Languages: Specific languages used to prepare computer programs.Angiotensin II: An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.ReadingFixation, Ocular: The positioning and accommodation of eyes that allows the image to be brought into place on the FOVEA CENTRALIS of each eye.Coitus Interruptus: A contraceptive method whereby coitus is purposely interrupted in order to prevent EJACULATION of SEMEN into the VAGINA.Cardiovascular Diseases: Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.Ramipril: A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.Stroke: A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)Hypertension: Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.Antihypertensive Agents: Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.Risk Factors: An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Blood Pressure Monitoring, Ambulatory: Method in which repeated blood pressure readings are made while the patient undergoes normal daily activities. It allows quantitative analysis of the high blood pressure load over time, can help distinguish between types of HYPERTENSION, and can assess the effectiveness of antihypertensive therapy.Myocardial Infarction: NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).Angioedema: Swelling involving the deep DERMIS, subcutaneous, or submucosal tissues, representing localized EDEMA. Angioedema often occurs in the face, lips, tongue, and larynx.Angioedemas, Hereditary: Inherited disorders that are characterized by subcutaneous and submucosal EDEMA in the upper RESPIRATORY TRACT and GASTROINTESTINAL TRACT.Hereditary Angioedema Types I and II: Forms of hereditary angioedema that occur due to mutations in the gene for COMPLEMENT C1 INHIBITOR PROTEIN. Type I hereditary angioedema is associated with reduced serum levels of complement C1 inhibitor protein. Type II hereditary angioedema is associated with the production of a non-functional complement C1 inhibitor protein.Complement C1 Inhibitor Protein: An endogenous 105-kDa plasma glycoprotein produced primarily by the LIVER and MONOCYTES. It inhibits a broad spectrum of proteases, including the COMPLEMENT C1R and the COMPLEMENT C1S proteases of the CLASSICAL COMPLEMENT PATHWAY, and the MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. C1-INH-deficient individuals suffer from HEREDITARY ANGIOEDEMA TYPES I AND II.Complement C1 Inactivator Proteins: Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.Electronic Prescribing: The use of COMPUTER COMMUNICATION NETWORKS to store and transmit medical PRESCRIPTIONS.Veterans: Former members of the armed services.Urticaria: A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress.Angiotensin Receptor Antagonists: Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.TaiwanRenin-Angiotensin System: A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.Perindopril: An angiotensin-converting enzyme inhibitor. It is used in patients with hypertension and heart failure.Cough: A sudden, audible expulsion of air from the lungs through a partially closed glottis, preceded by inhalation. It is a protective response that serves to clear the trachea, bronchi, and/or lungs of irritants and secretions, or to prevent aspiration of foreign materials into the lungs.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Asthma: A form of bronchial disorder with three distinct components: airway hyper-responsiveness (RESPIRATORY HYPERSENSITIVITY), airway INFLAMMATION, and intermittent AIRWAY OBSTRUCTION. It is characterized by spasmodic contraction of airway smooth muscle, WHEEZING, and dyspnea (DYSPNEA, PAROXYSMAL).Histamine: An amine derived by enzymatic decarboxylation of HISTIDINE. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.Lung: Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.Receptor, Angiotensin, Type 1: An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY, the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention.Bronchial Provocation Tests: Tests involving inhalation of allergens (nebulized or in dust form), nebulized pharmacologically active solutions (e.g., histamine, methacholine), or control solutions, followed by assessment of respiratory function. These tests are used in the diagnosis of asthma.Receptors, Angiotensin: Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.Holocaust: A massive slaughter, especially the systematic mass extermination of European Jews in Nazi concentration camps prior to and during World War II.Polymorphism, Genetic: The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.3-Oxoacyl-(Acyl-Carrier-Protein) Reductase: A 3-oxoacyl reductase that has specificity for ACYL CARRIER PROTEIN-derived FATTY ACIDS.Affect: The feeling-tone accompaniment of an idea or mental representation. It is the most direct psychic derivative of instinct and the psychic representative of the various bodily changes by means of which instincts manifest themselves.Electronic Mail: Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.Food Dispensers, Automatic: Mechanical food dispensing machines.Editorial Policies: The guidelines and policy statements set forth by the editor(s) or editorial board of a publication.Authorship: The profession of writing. Also the identity of the writer as the creator of a literary production.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Postal Service: The functions and activities carried out by the U.S. Postal Service, foreign postal services, and private postal services such as Federal Express.Legislation, Food: Laws and regulations concerned with industrial processing and marketing of foods.Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.Job Application: Process of applying for employment. It includes written application for employment or personal appearance.Fosinopril: A phosphinic acid-containing angiotensin-converting enzyme inhibitor that is effective in the treatment of hypertension. It is a prodrug that is converted to its active metabolite fosinoprilat.Bradykinin: A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.Swine, Miniature: Genetically developed small pigs for use in biomedical research. There are several strains - Yucatan miniature, Sinclair miniature, and Minnesota miniature.Atherosclerosis: A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.Iliac Artery: Either of two large arteries originating from the abdominal aorta; they supply blood to the pelvis, abdominal wall and legs.Angiotensins: Oligopeptides which are important in the regulation of blood pressure (VASOCONSTRICTION) and fluid homeostasis via the RENIN-ANGIOTENSIN SYSTEM. These include angiotensins derived naturally from precursor ANGIOTENSINOGEN, and those synthesized.Angiotensin I: A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.Butylated Hydroxyanisole: Mixture of 2- and 3-tert-butyl-4-methoxyphenols that is used as an antioxidant in foods, cosmetics, and pharmaceuticals.Angiotensin III: A heptapeptide formed from ANGIOTENSIN II after the removal of an amino acid at the N-terminal by AMINOPEPTIDASE A. Angiotensin III has the same efficacy as ANGIOTENSIN II in promoting ALDOSTERONE secretion and modifying renal blood flow, but less vasopressor activity (about 40%).Anisoles: A group of compounds that are derivatives of methoxybenzene and contain the general formula R-C7H7O.

Distinct and combined vascular effects of ACE blockade and HMG-CoA reductase inhibition in hypertensive subjects. (1/4593)

Hypercholesterolemia and hypertension are frequently associated with elevated sympathetic activity. Both are independent cardiovascular risk factors and both affect endothelium-mediated vasodilation. To identify the effects of cholesterol-lowering and antihypertensive treatments on vascular reactivity and vasodilative capacity, we studied 30 hypercholesterolemic hypertensive subjects. They received placebo for 4 weeks, either enalapril or simvastatin for 14 weeks, and, finally, both medications for an additional 14 weeks. Postischemic forearm blood flow (MFBF) and minimal vascular resistance (mFVR) were used as indices of vasodilative capacity and structural vascular damage, respectively. Total (resting-stress-recovery phases) cardiovascular (blood pressure [BP] and heart rate [HR]) and regional hemodynamic (FBF and FVR) reactivity to stressful stimuli were calculated as area-under-the-curve (auc) (valuextime). Compared with baseline levels, simvastatin reduced total (TOT-C) and LDL cholesterol (LDL-C) (1.27 mmol/L, P<0.001 and 1.33 mmol/L, P<0.001, respectively). Enalapril also reduced TOT-C and LDL-C (0.6 mmol/L, P<0.001 and 0.58 mmol/L, P<0.05, respectively). MFBF was increased substantially by both treatments (P<0.001). Enalapril had a greater effect (-1.7 arbitrary units (AU), P<0.001) than simvastatin (-0.6 AU, P<0.05) on mFVR. During stress, FBF increased more with enalapril (4.4 FBFxminutes, P<0.001) than with simvastatin (1.8 FBFxminutes, P<0.01). Conversely, FVR stress response was reduced more with enalapril (9.1 FVRxminutes, P<0.001) than with simvastatin (2.9 FVRxminutes, P<0.01). During combination treatment, a significant (0.001>P<0.05) additive effect on hypercholesterolemia, structural vascular damage, BP, and FVR was shown. The findings suggest that angiotensin-converting enzyme (ACE) inhibition induces a larger reduction than HMG-CoA reductase blockade in vascular reactivity and structural damage in hypercholesterolemic hypertensive subjects.  (+info)

Cardiac sympathetic activity estimated by 123I-MIBG myocardial imaging in patients with dilated cardiomyopathy after beta-blocker or angiotensin-converting enzyme inhibitor therapy. (2/4593)

Impaired cardiac sympathetic activity can be evaluated by 123I-metaiodobenzylguanidine (MIBG) imaging. METHODS: We studied the significance of MIBG imaging for 24 patients (age 58+/-12 y) with dilated cardiomyopathy (DCM). We compared 12 patients (group A) treated with metoprolol (dose from 30-60 mg/d) with 12 patients treated with angiotensin-converting enzyme (ACE) inhibitors. Patients were studied before treatment, after 5 mo of treatment (only in group A) and after 1 y of treatment. Cardiac MIBG uptake was assessed as the heart-to-mediastinum activity ratio (H/M) and total defect score (TDS) from anterior planar and SPECT MIBG images, which were acquired in 4 h after tracer injection. New York Heart Association (NYHA) class and left ventricular ejection fraction (LVEF) calculated by echocardiography were also assessed. RESULTS: TDS decreased in both groups (in group A, from 30+/-7 through 23+/-9 to 18+/-10; P < 0.01, in group B, from 30+/-6 to 24+/-8; P < 0.01) and H/M was increased in both groups (in group A, from 1.87+/-0.31 through 2.03+/-0.28 to 2.14+/-0.29; P < 0.01, in group B, from 1.82+/-0.28 to 1.94+/-0.26; P < 0.05). But TDS and H/M were more improved in group A than in group B (P < 0.05). LVEF was significantly increased in only group A (from 38+/-6 through 43+/-8 to 49%+/-9%; P < 0.01). NYHA improved in both groups (in group A, from mean 2.5 through 2.1 to 1.8; P < 0.01, in group B, from mean 2.6 to 2.1; P < 0.05) but was more improved in group A than in group B (P < 0.05). CONCLUSION: Cardiac function, symptom and cardiac sympathetic activity evaluated by MIBG images improved after the beta-blocker therapy more than with the treatment that used ACE inhibitors.  (+info)

Bradykinin promotes ischemic norepinephrine release in guinea pig and human hearts. (3/4593)

We previously reported that bradykinin (BK; 1-1000 nM) facilitates norepinephrine (NE) release from cardiac sympathetic nerves. Because BK production increases in myocardial ischemia, endogenous BK could foster NE release and associated arrhythmias. We tested this hypothesis in guinea pig and human myocardial ischemia models. BK administration (100 nM) markedly enhanced exocytotic and carrier-mediated NE overflow from guinea pig hearts subjected to 10- and 20-min ischemia/reperfusion, respectively. Ventricular fibrillation invariably occurred after 20-min global ischemia; BK prolonged its duration 3-fold. The BK B2 receptor antagonist HOE140 (30 nM) blocked the effects of BK, whereas the B1 receptor antagonist des-Arg9-Leu8-BK (1 microM; i.e., 2.5 x pA2) did not. When serine proteinase inhibitors (500 KIU/ml aprotinin and 100 microg/ml soybean trypsin inhibitor) were used to prevent the formation of endogenous BK, NE overflow and reperfusion arrhythmias were diminished. In contrast, when kininase I and II inhibitors (DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid and enalaprilat, each 1 microM) were used to prevent the degradation of endogenous BK, NE overflow and reperfusion arrhythmias were enhanced. B2 receptor blockade abolished these effects but was ineffective if kininases were not inhibited. B2 receptor stimulation, by either exogenous or endogenous BK, also markedly enhanced carrier-mediated NE release in the human myocardial ischemia model; conversely, inhibition of BK biosynthesis diminished ischemic NE release. Because atherosclerotic heart disease impairs endothelial BK production, in myocardial ischemia BK could accumulate at sympathetic nerve endings, thus augmenting exocytotic and carrier-mediated NE release and favoring coronary vasoconstriction and arrhythmias.  (+info)

Blocking angiotensin II ameliorates proteinuria and glomerular lesions in progressive mesangioproliferative glomerulonephritis. (4/4593)

BACKGROUND: The renin-angiotensin system is thought to be involved in the progression of glomerulonephritis (GN) into end-stage renal failure (ESRF) because of the observed renoprotective effects of angiotensin-converting enzyme inhibitors (ACEIs). However, ACEIs have pharmacological effects other than ACE inhibition that may help lower blood pressure and preserve glomerular structure. We previously reported a new animal model of progressive glomerulosclerosis induced by a single intravenous injection of an anti-Thy-1 monoclonal antibody, MoAb 1-22-3, in uninephrectomized rats. Using this new model of progressive GN, we examined the hypothesis that ACEIs prevent the progression to ESRF by modulating the effects of angiotensin II (Ang II) on the production of transforming growth factor-beta (TGF-beta) and extracellular matrix components. METHODS: We studied the effect of an ACEI (cilazapril) and an Ang II type 1 receptor antagonist (candesartan) on the clinical features and morphological lesions in the rat model previously reported. After 10 weeks of treatment with equihypotensive doses of cilazapril, cilazapril plus Hoe 140 (a bradykinin receptor B2 antagonist), candesartan, and hydralazine, we examined systolic blood pressure, urinary protein excretion, creatinine clearance, the glomerulosclerosis index, and the tubulointerstitial lesion index. We performed a semiquantitative evaluation of glomerular immunostaining for TGF-beta and collagen types I and III by immunofluorescence study and of these cortical mRNA levels by Northern blot analysis. RESULTS: Untreated rats developed massive proteinuria, renal dysfunction, and severe glomerular and tubulointerstitial injury, whereas uninephrectomized control rats did not. There was a significant increase in the levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III in untreated rats. Cilazapril and candesartan prevented massive proteinuria, increased creatinine clearance, and ameliorated glomerular and tubulointerstitial injury. These drugs also reduced levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III. Hoe 140 failed to blunt the renoprotective effect of cilazapril. Hydralazine did not exhibit a renoprotective effect. CONCLUSION: These results indicate that ACEIs prevent the progression to ESRF by modulating the effects of Ang II via Ang II type 1 receptor on the production of TGF-beta and collagen types I and III, as well as on intrarenal hemodynamics, but not by either increasing bradykinin activity or reducing blood pressure in this rat model of mesangial proliferative GN.  (+info)

Glomerular size-selective dysfunction in NIDDM is not ameliorated by ACE inhibition or by calcium channel blockade. (5/4593)

BACKGROUND: In patients with insulin-dependent diabetes mellitus (IDDM) and overt nephropathy glomerular barrier size-selectivity progressively deteriorates with time and is effectively improved by angiotensin converting enzyme (ACE) inhibition. Whether similar glomerular functional changes develop in proteinuric patients with non-insulin-dependent diabetes mellitus (NIDDM), and whether antihypertensive agents can favorably affect glomerular filtration of macromolecules in these patients, has not been documented yet. METHODS: We investigated renal hemodynamics and fractional clearance of neutral dextrans of graded sizes, in nine proteinuric patients with NIDDM and renal biopsy findings of typical diabetic glomerulopathy. Six healthy volunteers served as controls. We also investigated the effects of an ACE inhibitor and of a calcium channel blocker, both given in doses targeted to achieve a comparable level of systemic blood pressure control, on glomerular hemodynamics and sieving function. Theoretical analysis of glomerular macromolecule transport was adopted to evaluate intrinsic glomerular membrane permeability properties. RESULTS: Fractional clearance of large macromolecules (42 to 66 A in radius) was significantly higher in diabetic patients than in controls, and the distribution of membrane pore radii was calculated to be shifted towards larger pore sizes in diabetics (mean radius increased from 55 to 60 A). Despite effective blood pressure control, neither antihypertensive affected glomerular hemodynamics to any significant extent. Fractional clearance of dextrans, as well as of albumin and IgG, and total urinary proteins were not modified by either treatments. CONCLUSIONS: These data indicate that patients with NIDDM and overt nephropathy develop abnormalities in size-selective function of the glomerular barrier and, at variance to IDDM, such changes were not ameliorated either by ACE inhibition or calcium channel blockade.  (+info)

Racial differences in the outcome of left ventricular dysfunction. (6/4593)

BACKGROUND: Population-based studies have found that black patients with congestive heart failure have a higher mortality rate than whites with the same condition. This finding has been attributed to differences in the severity, causes, and management of heart failure, the prevalence of coexisting conditions, and socioeconomic factors. Although these factors probably account for some of the higher mortality due to congestive heart failure among blacks, we hypothesized that racial differences in the natural history of left ventricular dysfunction might also have a role. METHODS: Using data from the Studies of Left Ventricular Dysfunction (SOLVD) prevention and treatment trials, in which all patients received standardized therapy and follow-up, we conducted a retrospective analysis of the outcomes of asymptomatic and symptomatic left ventricular systolic dysfunction among black and white participants. The mean (+/-SD) follow-up was 34.2+/-14.0 months in the prevention trial and 32.3+/-14.8 months in the treatment trial among the black and white participants. RESULTS: The overall mortality rates in the prevention trial were 8.1 per 100 person-years for blacks and 5.1 per 100 person years for whites. In the treatment trial, the rates were 16.7 per 100 person-years and 13.4 per 100 person-years, respectively. After adjustment for age, coexisting conditions, severity and causes of heart failure, and use of medications, blacks had a higher risk of death from all causes in both the SOLVD prevention trial (relative risk, 1.36; 95 percent confidence interval, 1.06 to 1.74; P=0.02) and the treatment trial (relative risk, 1.25; 95 percent confidence interval, 1.04 to 1.50; P=0.02). In both trials blacks were also at higher risk for death due to pump failure and for the combined end point of death from any cause or hospitalization for heart failure, our two predefined indicators of the progression of left ventricular systolic dysfunction. CONCLUSIONS: Blacks with mild-to-moderate left ventricular systolic dysfunction appear to be at higher risk for progression of heart failure and death from any cause than similarly treated whites. These results suggest that there may be racial differences in the outcome of asymptomatic and symptomatic left ventricular systolic dysfunction.  (+info)

Reduction of sodium deoxycholic acid-induced scratching behaviour by bradykinin B2 receptor antagonists. (7/4593)

1. Subcutaneous injection of sodium deoxycholic acid into the anterior of the back of male ddY mice elicited dose-dependent scratching of the injected site with the forepaws and hindpaws. 2. Up to 100 microg of sodium deoxycholic acid induced no significant increase in vascular permeability at the injection site as assessed by a dye leakage method. 3. Bradykinin (BK) B2 receptor antagonists, FR173657 and Hoe140, significantly decreased the frequency of scratching induced by sodium deoxycholic acid. 4. Treatment with aprotinin to inhibit tissue kallikrein reduced the scratching behaviour induced by sodium deoxycholic acid, whereas treatment with soybean trypsin inhibitor to inhibit plasma kallikrein did not. 5. Although injection of kininase II inhibitor, lisinopril together with sodium deoxycholic acid did not alter the scratching behaviour, phosphoramidon, a neutral endopeptidase inhibitor, significantly increased the frequency of scratching. 6. Homogenates of the skin excised from the backs of mice were subjected to gel-filtration column chromatography followed by an assay of kinin release by trypsin from each fraction separated. Less kinin release from the fractions containing kininogen of low molecular weight was observed in the skin injected with sodium deoxycholic acid than in normal skin. 7. The frequency of scratching after the injection of sodium deoxycholic acid in plasma kininogen-deficient Brown Norway Katholiek rats was significantly lower than that in normal rats of the same strain, Brown Norway Kitasato rats. 8. These results indicate that BK released from low-molecular-weight kininogen by tissue kallikrein, but not from high-molecular-weight kininogen by plasma kallikrein, may be involved in the scratching behaviour induced by the injection of sodium deoxycholic acid in the rodent.  (+info)

Addition of angiotensin II receptor blockade to maximal angiotensin-converting enzyme inhibition improves exercise capacity in patients with severe congestive heart failure. (8/4593)

BACKGROUND: Incomplete suppression of the renin-angiotensin system during long-term ACE inhibition may contribute to symptomatic deterioration in patients with severe congestive heart failure (CHF). Combined angiotensin II type I (AT1) receptor blockade and ACE inhibition more completely suppresses the activated renin-angiotensin system than either intervention alone in sodium-depleted normal individuals. Whether AT1 receptor blockade with losartan improves exercise capacity in patients with severe CHF already treated with ACE inhibitors is unknown. METHODS AND RESULTS: Thirty-three patients with severe CHF despite treatment with maximally recommended or tolerated doses of ACE inhibitors were randomized 1:1 to receive 50 mg/d losartan or placebo for 6 months in addition to standard therapy in a multicenter, double-blind trial. Peak aerobic capacity (V(O2)) during symptom-limited treadmill exercise and NYHA functional class were determined at baseline and after 3 and 6 months of double-blind therapy. Peak V(O2) at baseline and after 3 and 6 months were 13.5+/-0.6, 15.1+/-1.0, and 15.7+/-1.1 mL. kg-1. min-1, respectively, in patients receiving losartan and 14.1+/-0.6, 14.3+/-0.9, and 13.6+/-1.1 mL. kg-1. min-1, respectively, in patients receiving placebo (P<0.02 for treatment group-by-time interaction). Functional class improved by at least one NYHA class in 9 of 16 patients receiving losartan and 1 of 17 patients receiving placebo. CONCLUSIONS: Losartan enhances peak exercise capacity and alleviates symptoms in patients with CHF who are severely symptomatic despite treatment with maximally recommended or tolerated doses of ACE inhibitors.  (+info)

*Angiotensin-converting enzyme 2

... is a novel mammalian metallocarboxypeptidase and a homologue of angiotensin-converting enzyme insensitive to ACE inhibitors". ... "A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9". Circulation ... "A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9". Circulation ... Angiotensin converting enzyme 2 (ACE 2) is an exopeptidase that catalyses the conversion of angiotensin I to the nonapeptide ...

*Angiotensin II receptor type 1

... angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are associated with fewer traumatic stress symptoms ... Angiotensin II receptor type 1 or AT1 receptor is the best characterized angiotensin receptor. It has vasopressor effects and ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... Angiotensin II receptor type 1 has been shown to interact with Zinc finger and BTB domain-containing protein 16. The protein's ...

*Captopril challenge test

... an angiotensin converting enzyme inhibitor. It is used to assist in the diagnosis of renal artery stenosis. It is not generally ...

*Captopril

... , sold under the trade name Capoten, is an angiotensin-converting enzyme (ACE) inhibitor used for the treatment of ... Brown, NJ; Vaughan, DE (1998). "Angiotensin-converting enzyme inhibitors". Circulation. 97 (14): 1411-20. doi:10.1161/01.cir. ... "Design of specific inhibitors of angiotensin-converting enzyme: New class of orally active antihypertensive agents". Science. ... "A new class of angiotensin-converting enzyme inhibitors". Nature. 288 (5788): 280-3. doi:10.1038/288280a0. PMID 6253826. " ...

*Redback spider

Angiotensin-converting-enzyme inhibitors, or ACE inhibitors, are a class of widely-prescribed medications used in hypertension ... Sweitzer, Nancy K. (2003). "What Is an Angiotensin Converting Enzyme Inhibitor?". Circulation. 108 (3): e16-18. doi:10.1161/01. ... as have small peptides that inhibit angiotensin-1-converting enzyme; the venom of the redback, although little-studied, likely ... It contains a complex mixture of cellular constituents, enzymes and a number of high-molecular-weight toxins, including insect ...

*Lisinopril

... is an ACE Inhibitor, meaning it blocks the actions of angiotensin converting enzyme (ACE) in the renin-angiotensin- ... Lisinopril is a drug of the angiotensin-converting enzyme (ACE) inhibitor class used primarily in treatment of high blood ... John Wiley & Sons, Apr 3, 2013 ISBN 9781118354469 Menard J and Patchett A. "Angiotensin-Converting Enzyme Inhibitors". pp. 14- ... 1980). "A new class of angiotensin-converting enzyme inhibitors". Nature. 288 (5788): 280-3. Bibcode:1980Natur.288..280P. doi: ...

*Natural product

These include the angiotensin-converting enzyme inhibitor captopril. Captopril is based on the peptidic bradykinin potentiating ... Enzymes in turn are composed of amino acids and often non-peptidic cofactors that are essential for enzyme function. The basic ... In animals, the three carbon precursors lactate or glycerol can be converted into pyruvate which in turn can be converted into ... they possess enzymes that are functional under quite unusual conditions. These enzymes are of potential use in the food, ...

*Ecallantide

"Ecallantide for the acute treatment of Angiotensin-converting enzyme inhibitor-induced angioedema: a multicenter, randomized, ... "Pharmacologic management of angioedema induced by angiotensin-converting enzyme inhibitors". American Journal of Health-System ... HAE is caused by a mutation of the C1-inhibitor gene. Defective or missing C1-inhibitor permits activation of kallikrein, a ... It is an inhibitor of the protein kallikrein and a 60-amino acid polypeptide which was developed from a Kunitz domain through ...

*Teprotide

It is an angiotensin converting enzyme inhibitor (ACE inhibitor), which inhibits the conversion of angiotensin I to angiotensin ... It was found that teprotide inhibits the enzyme that converts angiotensin I to angiotensin II. From this researchers conducted ... "Angiotensin-converting enzyme inhibitors from the venom of bothrops jararaca. Isolation, elucidation of structure, and ... "History of the design of captopril and related inhibitors of angiotensin converting enzyme". Hypertension. 17 (4): 589-592. doi ...

*Rentiapril

Takase K, Ikuse T, Aono H, Okahara A (January 1995). "Toxicity study of the angiotensin converting enzyme inhibitor rentiapril ...

*Miguel Ondetti

Ondetti started work on the isolation of angiotensin-converting enzyme inhibitors. By 1973, work on ACE inhibitors stopped ... Ondetti M A, Rubin B, Cushman D W. Design of specific inhibitors of angiotensin-converting enzyme: new class of orally active ... Ondetti M A, Sabo E F. Angiotensin-converting enzyme inhibitors from the venom of Bothrops jararaca. Isolation, elucidation of ... In 1974, Ondetti resumed unofficial work on ACE inhibitors with strong resolve, "We said this was the thing that we had to do ...

*Tricuspid insufficiency

Medications in this case may include diuretics and angiotensin-converting enzyme inhibitors. The prognosis of tricuspid ...

*Moexipril

... hydrochloride is a potent orally active nonsulfhydryl angiotensin converting enzyme inhibitor (ACE inhibitor) which ... Chrysant, S. G. (1998). "Vascular remodeling: The role of angiotensin-converting enzyme inhibitors". American Heart Journal. ... "Synthesis of novel angiotensin converting enzyme inhibitor quinapril and related compounds. A divergence of structure-activity ... AN IMPORTANT INTERMEDIATE IN THE SYNTHESIS OF ANGIOTENSIN CONVERTING ENZYME INHIBITORS". Organic Preparations and Procedures ...

*Angioedema

"Investigation of angioedema associated with the use of angiotensin-converting enzyme inhibitors and angiotensin receptor ... Sabroe RA, Black AK (February 1997). "Angiotensin-converting enzyme (ACE) inhibitors and angio-oedema". British Journal of ... Israili ZH, Hall WD (August 1, 1992). "Cough and angioneurotic edema associated with angiotensin-converting enzyme inhibitor ... Dykewicz, MS (August 2004). "Cough and angioedema from angiotensin-converting enzyme inhibitors: new insights into mechanisms ...

*First-dose phenomenon

... angiotensin-converting enzyme inhibitor). This may occur with the class's better known side effect of dry cough (due to ... www.medicinescomplete.com/mc/bnf/current/PHP1124-angiotensin-converting-enzyme-inhibitors.htm. ...

*Enalapril

It is in the angiotensin-converting-enzyme inhibitor (ACEi) family of medications. Enalapril was patented in 1978 and came into ... Normally, angiotensin I is converted to angiotensin II by an angiotensin-converting enzyme (ACE). Angiotensin II constricts ... Last updated April 2011 Menard J and Patchett A. Angiotensin-Converting Enzyme Inhibitors. Pp 14-76 in Drug Discovery and ... Jenny Bryan for The Pharmaceutical Journal, 17 Apr 2009 From snake venom to ACE inhibitor - the discovery and rise of captopril ...

*Drug eruption

Angioedema can also be drug-induced (most notably, by angiotensin converting enzyme inhibitors). The underlying mechanism can ... of SJS or TEN compared to the general population and have been found to express low levels of the drug metabolizing enzyme ...

*TRPA1

"Identification of genetic factors associated with susceptibility to angiotensin-converting enzyme inhibitors-induced cough". ... 12S-HpETE, which is the direct precursor to HxA3 and HxB3 in the ALOX12 pathway, may act only after being converted to these ... Genetic polymorphism in the EP3 receptor (rs11209716), has been associated with ACE inhibitor-induce cough in humans. Resolvin ... made by the metabolism of arachidonic acid by any one of several cytochrome P450 enzymes (see Epoxyeicosatrienoic acid) ...

*Prostaglandin EP3 receptor

"Identification of genetic factors associated with susceptibility to angiotensin-converting enzyme inhibitors-induced cough". ... The ability of endotoxind and IL-1β but not that of PGE2 to trigger fever is blocked by inhibitors of nitric oxide and PG2 EP33 ... Genetic polymorphism in the EP3 receptor (rs11209716), has been associated with ACE inhibitor-induce cough in humans. The use ... pathways that activate phospholipase C to convert cellular phospholipids to diacylglycerol which promotes the activation of ...

*Benazepril

Dykewicz, Mark S. (April 2004). "Cough and Angioedema From Angiotensin-Converting Enzyme Inhibitors: New Insights Into ... They inhibit angiotensin-converting enzyme, which is part of the renin-angiotensin-aldosterone system. Benazepril is a prodrug ... and inhibition of plasma angiotensin-converting enzyme activity after single and repeated administrations to dogs". Am. J. Vet ... ACE inhibitors relax blood vessels, and decrease blood volume, which lowers blood pressure and decreases oxygen demand from the ...

*Carboxylesterase 1

CES1 is responsible for the activation of many prodrugs such as angiotensin-converting enzyme (ACE) inhibitors, oseltamivir, ... focus on angiotensin-converting enzyme inhibitors". Drug Metab Dispos. 42 (1): 126-33. doi:10.1124/dmd.113.053512. PMID ... These enzymes are responsible for the hydrolysis of ester- and amide-bond-containing xenobiotics and drugs such as cocaine and ... This enzyme is known to hydrolyze aromatic and aliphatic esters and can manage cellular cholesterol esterification levels. It ...

*Polycystic kidney disease

Hypertension is treated with angiotensin converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs). ... Complications include hypertension due to the activation of the renin-angiotensin-aldosterone system (RAAS), frequent cyst ...

*Short linear motif

For example, Tritace®, Vasotec®, Accupril®, and Lotensin® are substrate mimetic Angiotensin converting enzymes inhibitors. ... Many classes of ligand SLiMs recruit enzymes to their substrate by binding to sites that are distinct from the enzyme's active ... an antiviral myristoylation inhibitor and Farnysyl Transferase inhibitors that block the lipidation modification to a CAAX-box ... Goodman SL, Hölzemann G, Sulyok GA, Kessler H (2002). "Nanomolar small molecule inhibitors for alphav(beta)6, alphav(beta)5, ...

*TRPV1

"Identification of genetic factors associated with susceptibility to angiotensin-converting enzyme inhibitors-induced cough". ... AM404-an active metabolite of paracetamol-that serves as an anandamide reuptake inhibitor and COX inhibitor also serves as a ... Genetic polymorphism in the EP3 receptor (rs11209716), has been associated with ACE inhibitor-induced cough in humans. Resolvin ... "Systematic analysis of rat 12/15-lipoxygenase enzymes reveals critical role for spinal eLOX3 hepoxilin synthase activity in ...

*Ramipril

ACE inhibitors inhibit the actions of angiotensin converting enzyme (ACE), thereby lowering the production of angiotensin II ... Angiotensin-converting enzyme (ACE) inhibitor Hypertension Hypotension Heart failure Chest pain Pilote L; Abrahamowicz M; ... Ramipril, sold under the brand name Altace among others, is an angiotensin-converting enzyme (ACE) inhibitor, used to treat ... Jan 2014). "In vitro drug metabolism by human carboxylesterase 1: focus on angiotensin-converting enzyme inhibitors". Drug ...

*Aspiration pneumonia

... proton pump inhibitors, and angiotensin-converting enzyme inhibitors. Reduced functional status, residence in an institutional ...

*Icatibant

undefined NaN). "Randomized Trial of Icatibant for Angiotensin-Converting Enzyme Inhibitor-Induced Upper Airway Angioedema". ... in adults with C1-esterase-inhibitor deficiency. It is not effective in angioedema caused by medication from the ACE inhibitor ... Icatibant acts as a bradykinin inhibitor by blocking the binding of native bradykinin to the bradykinin B2 receptor. Icatibant ...
2017 The Author. Published by Oxford University Press for the Infectious Diseases Society of America. Background. Although statins, angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB) are generally well tolerated, the impact of these therapies individually or in combination on the change in neurocognitive function in persons with human immunodeficiency virus infection is unknown. Methods. The study included participants in the AIDS Clinical Trials Group Longitudinal Linked Randomized Trials cohort participants not receiving a statin or ACEI/ARB within 30 days of first neurologic assessment (baseline), with assessments by NPZ-3 (z score of averaged Trailmaking A and B tests and digit symbol test [DST]) from ≥2 measurements. Marginal structural models estimated the causal effect of statin or ACEI/ARB initiation on neurocognitive function; initial constant slope was assumed during the first year of treatment and a second constant slope thereafter. Results. Of ...
Dr. James Lohr, Division of Nephrology, VAMC, 3495 Bailey Avenue, Buffalo, NY 14215. Phone: 716-862-3204; Fax: 716-862-6784; E-mail: James.Lohr{at}med.va.gov ...
Background. Renal function decreases with age. Dosage adjustment according to renal function is indicated for many drugs, in order to avoid adverse reactions of medications and/or aggravation of renal impairment. There are several ways to assess renal function in the elderly, but no way is ideal. The aim of the study was to explore renal function in elderly subjects in nursing homes and the use of pharmaceuticals that may be harmful to patients with renal impairment.. Methods. 243 elderly subjects living in nursing homes were included. S-creatinine and s-cystatin c were analysed. Renal function was estimated using Cockcroft-Gault formula, Modification of Diet in Renal Disease (MDRD) and cystatin C-estimated glomerular filtration rate (GFR). Concomitant medication was registered and four groups of renal risk drugs were identified: metformin, nonsteroidal anti-inflammatory drugs (NSAID), angiotensin-converting enzyme -inhibitors/angiotensin receptor blockers and digoxin. Descriptive statistics and ...
Our results demonstrate that good adherence to statin in the first 6 months after discharge is associated with subsequent lower incidence of MACE (including all-cause mortality, MI, and stroke) in a large unselected Chinese ACS patient population. This relationship was independent of other treatments which have been shown to be associated with outcomes in ACS such as receipt of coronary interventions, and adherence to antiplatelets, aspirin, beta-blocker, and angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, as well as other known personal prognostic factors such as age, sex, education level, and cardiovascular risk factors and other hospital level characteristics. In addition, the effect of adherence was not modified by the characteristics of patients such as dose of statins, subtypes of ACS, gender, age, social economic status, etc.. It has been well established that good statin adherence is associated with reduced the risk of MACE and all-cause mortality in the primary ...
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Angiotensin I-converting enzyme (ACE) inhibitory activity was investigated for small red bean (Phaseolus vulgaris) protein hydrolysate produced by sequential digestion of Alcalase, papain followed by in vitro gastrointestinal simulation. The hydrolysate had ACE inhibitory activity with IC50 of 67.2 ± 1.8 μg protein/mL. Peptides responsible for potent ACE inhibitory activity were isolated by a three-step purification process, including ultrafiltration, gel filtration and preparative reverse phase high performance chromatography (RP-HPLC). The fraction obtained after RP-HPLC fractionation with the highest activity yielded an IC50 of 19.3 ± 1.4 μg protein/mL. Enzymatic kinetic studies using this fraction demonstrated competitive inhibition with Ki of 11.6 ± 1.7 μg protein/mL. Mass spectrometric characterization identified for the first time the octapeptide PVNNPQIH which demonstrated an IC50 value of 206.7 ± 3.9 μM. The results expand the knowledge base of ACE inhibitory properties of small ...
OBJECTIVES: We sought to determine whether the clinical effects of early angiotensin-converting enzyme (ACE) inhibitor (ACEi) treatment for acute myocardial infarction (MI) are influenced by the concomitant use of aspirin (ASA). BACKGROUND: Aspirin a
Purpose Renin-angiotensin system blockers (RASBs), which include angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin-2 receptor 1 blockers (ARBs), have been reported to be associated with lung cancer metastasis, radiotherapy and chemotherapy. Until now, very limited clinical data for RASBs diagnostic and prognostic effects has existed for lung cancer chemotherapy in Chinese patients. Methods There were a total of 678 lung cancer patients with hypertension, of which 461 (68%) were in the non-RASBs group and 217 (32%) were in the RASBs group. Patients gender, age, smoking status, histologic differentiation, tumor size, pathological grade, lymph node metastasis, pathological stage and progression-free survival (PFS) were retrospectively analyzed between these two groups. The clinical effects of ACEIs and ARBs in lung cancer patients were compared via t tests, and χ2 test, and potential prognostic factors for progression-free survival (PFS) were evaluated by Kaplan-Meier analysis. Results
The major new finding of the present study is that Hoe140, a bradykinin BK2-receptor antagonist, inhibited the captopril-induced change in CBF autoregulation. The result suggests that the modulation of CBF autoregulation by captopril is mediated, at least in part, by bradykinin.. In a previous report, in which Hoe140 (0.75 nmol) was infused into the aorta in Sprague-Dawley rats, bradykinin-induced hypotension was still impaired by 71% 1 hour after infusion.13 In the present intravenous study, the dose of Hoe140 was similar to or even greater than that in the previous study, and it completely prevented the hypotensive effect of bradykinin. In a steady state, Hoe140 concentration in the circulating blood should be constant in the whole body, including cerebral vessels. This means that a sufficient concentration of Hoe140 to block BK2 receptors should have reached cerebral arteries during the experiment. Furthermore, there is no report that the distribution of BK2 receptor is different between ...
How does angiotensin-converting enzyme inhibitors ace inhibitors work with other drugs and supplements? Helpful and harmful angiotensin-converting enzyme...
The review addressed a clear question for which inclusion criteria were defined. However, decisions to exclude studies from the review might have been subject to bias, as the criteria for exclusion appear to have been defined after the retrieval of primary studies. Attempts were made to locate unpublished studies in the search for primary studies, though a number of unpublished studies were excluded as the data could not be obtained. Funnel plots suggested evidence of publication bias. It was unclear whether steps were taken to minimise bias and errors in the study selection and data extraction as these processes were not described. The authors stated that they did not assess study quality since the included studies were all double-blind RCTs of a similar design, but it would appear from comments in the discussion that the studies had several methodological limitations.. The statistical techniques used to combine the studies and to investigate heterogeneity were applied appropriately, and ...
Is primary indication for ACE inhibitor the treatment of the patients with AMI syndrome or with LV dysfunction that at any time complicates AMI? In the first case, should all patients or only those at higher risk be treated (ie, anterior AMI, large AMI)?. When should ACE inhibitor treatment be started?. The two questions are presented together because the answer to question 1 is integrally related to question 2. The evidence available from the trials on ACE inhibitors is documented in detail in Tables 1⇑ and 2⇑ and may be summarized as follows. Treatment with ACE inhibitors has a beneficial effect in patients selected for the presence of LV dysfunction after AMI and in relatively unselected patients presenting with AMI. The benefit increases in patients with clinical or laboratory evidence of LV dysfunction. There is still uncertainty about treating all AMI patients without contraindications to ACE inhibitors or targeting a selected higher-risk group.. The extension of the indication of ...
TY - JOUR. T1 - Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers in Myocardial Infarction. AU - Kostis, John. PY - 2019/7/1. Y1 - 2019/7/1. UR - http://www.scopus.com/inward/record.url?scp=85065221731&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=85065221731&partnerID=8YFLogxK. U2 - https://doi.org/10.1177/1074248419841636. DO - https://doi.org/10.1177/1074248419841636. M3 - Letter. C2 - 31035789. VL - 24. JO - Journal of Cardiovascular Pharmacology and Therapeutics. JF - Journal of Cardiovascular Pharmacology and Therapeutics. SN - 1074-2484. IS - 4. ER - ...
The background for these investigations was the discovery that formation of angiotensin II by the renin angiotensin system can take place in extravascular tissues (e.g., cardiomyocytes and neurons) and within single cells. Consequently, the question arose about whether such tissue-based systems might be differentially influenced by angiotensin I-converting enzyme (ACE) inhibitors with distinct physicochemical properties. Therefore, the aim of this study was to investigate how the membrane penetration of various ACE inhibitors depends on their lipophilia. All diacid forms of ACE inhibitors are dissociated at a pH of 7.4 and scarcely extractable into octanol (extraction coefficient ,10%). In contrast, the extraction coefficients of the parent substances showed marked differences in the following order of increasing lipophilia: enalapril=perindopril,captopril=ceranapril,ramipril,quinapril,HOE288=zofenopril,fosinopril,HOE065. For selected substances, the kinetics of diffusion through a monolayer of ...
The main result of this study is that ACE inhibition enhances ischemia-induced angiogenesis through the activation of the B2-receptor pathway. This proangiogenic effect may be associated with the upregulation of eNOS expression but seems independent of the VEGF pathway.. Although evidence is accumulating on the activating role of ACE inhibition in vessel growth, little is known about the cellular signaling involved in such an angiogenic effect. Our study confirms that ACE inhibition enhanced revascularization of the ischemic hindlimb but demonstrates that such an effect was mediated by B2-receptor activation. Indeed, ACE inhibition did not affect vessel growth in mice lacking B2 receptor. Similarly, long-term B2-receptor blockade prevented the ACE inhibitor-induced increase in cardiac capillary density in stroke-prone spontaneously hypertensive rats.8 In the same view, long-term ACE inhibitor treatment ameliorated the severity of myocardial injury in cholesterol-fed rabbits via B2 ...
Angiotensin-converting enzyme inhibitors (ACEi) are commonly used for pediatric cardiology patients. However, studies examining their safety for neonates with cardiac disease are scarce. The current study aimed to test the hypothesis that ACEi-mediated nephrotoxicity occurs in neonates and may be underappreciated in this population. A retrospective review of 243 neonates with cardiac disease between 2007 and 2010 was performed. Demographic data, weight, length, captopril and enalapril dosing, serum [K⁺], serum creatinine, and concomitant medications during ACEi therapy were recorded and analyzed. Body surface area (BSA), creatinine clearance (CrCl), and change in [K⁺] were calculated. The age range of neonates at ACEi initiation was 15.9-18.1 days. The inclusion criteria was met by 206 neonates: 168 term (82%) and 38 preterm (18%) newborns. Of these neonates, 42% were female, and all the patients had a BSA smaller than 0.33 m² (a group known to have relative renal insufficiency). The mean ...
BACKGROUND: Results from a retrospective analysis of the Studies of Left Ventricular Dysfunction (SOLVD) study suggest that angiotensin-converting-enzyme (ACE) inhibitors may be less effective in patients receiving aspirin. We aimed to confirm or refute this theory. METHODS: We used the Peto-Yusuf method to undertake a systematic overview of data for 22060 patients from six long-term randomised trials of ACE inhibitors to assess whether aspirin altered the effects of ACE inhibitor therapy on major clinical outcomes (composite of death, myocardial infarction, stroke, hospital admission for congestive heart failure, or revascularisation). FINDINGS: Baseline characteristics, and prognosis in patients allocated placebo, differed strikingly between those who were and were not taking aspirin at baseline. Results from analyses of all trials, except SOLVD, did not suggest any significant differences between the proportional reductions in risk with ACE inhibitor therapy in the presence or absence of aspirin for
For ischemic heart disease with refractory angina that cannot be revascularized, Dr. Miller said options include optimizing medical therapy, such as beta-blockers, calcium channel blockers, nitrates, ranolazine, allopurinol, L-arginine, opioids, and perhaps some investigational agents (if you can get the patient enrolled in a clinical trial). In this setting, the heart team may include the patients general cardiologist, primary doctor, family, nurses, and perhaps other office staff.. While the medical record may suggest the patient is on appropriate therapy, adherence may be a factor. After MI, a large proportion of patients discontinue use of medications over time. Indeed, by 3 years, more than half of patients in one community-based study had already stopped taking statins, beta-blockers, or angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers.4. Also, its important to target risk factors through statin therapy, antihypertensives, antiplatelets, smoking cessation, weight ...
Angiotensin-II receptor antagonists (or blockers) are a newer class of antihypertensive agents. These drugs are selective for angiotensin II (type 1 receptor); unlike angiotensin-converting enzyme inhibitors, they do not inhibit bradykinin metabolism or enhance prostaglandin synthesis. Angiotensin-II receptor antagonists are well tolerated. Cough occurs much less often with these agents than with angiotensin-converting enzyme inhibitors, and they do not adversely affect lipid profiles or cause rebound hypertension after discontinuation. Clinical trials indicate that angiotensin-II receptor antagonists are effective and safe in the treatment of hypertension. Their use in congestive heart failure and renal disease is under investigation.
Learn more about Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors) at Aventura Hospital & Medical Center Arginine -Possible Harmful Interaction ...
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Long-term therapy with an angiotensin-converting enzyme (ACE) inhibitor appears to reduce urinary albumin excretion and improve lipid metabolism in patients with hypertension, research findings suggest. As physicians come to understand the role of ACE inhibitors in hypertension, the long-term view is showing the
PubMed journal article Beyond ONTARGET: angiotensin-converting enzyme inhibition and angiotensin II receptor blockade in combination, a lesser evil in some? were found in PRIME PubMed. Download Prime PubMed App to iPhone or iPad.
Several well-controlled trials in patients with heart failure have shown that the use of angiotensin-converting enzyme (ACE) inhibitors, in combination with a diuretic, causes a reduction in mortality and morbidity, which seems to be mainly due to a reduction in fatal and nonfatal cardiovascular events. Our aim was to determine whether 249 consecutive patients discharged from hospital with a primary diagnosis of heart failure were routinely being treated with an ACE inhibitor at an appropriate dose. At the time of admission to hospital, 91 (36.5%) were receiving a combination of a diuretic and an ACE inhibitor, 129 (51.8%) were receiving a diuretic alone, and 29 (11.6%) had not previously received either a diuretic or an ACE inhibitor. At the time of discharge from hospital all patients were on a diuretic and 144 (57.8%) were also receiving an ACE inhibitor. Although 41 patients (16.5%) had a relative or absolute contraindication for the use of an ACE inhibitor, 64 patients (25.7%) with no ...
β-Adrenergic desensitization has been suggested to represent an important mechanism of contractile dysfunction in heart failure.11 12 13 14 15 16 The diminished formation of the second-messenger cAMP after stimulation of cardiac β-adrenergic receptors is due to a decline in the number of β-adrenergic receptors,11 12 13 an uncoupling of β-adrenergic receptors, and an increase in inhibitory G protein α subunits.14 15 16 The underlying mechanism inducing these desensitization processes is an activation of the sympathetic nervous system and, in particular, sympathetic activation in the heart itself.2 Several reports indicate that β-adrenergic neuroeffector defects occur not only in terminal heart failure but also in hypertensive heart disease.37 These data have been obtained in rat models of hypertensive heart disease (eg, spontaneously hypertensive rats38 39 ), rat models of acquired forms of hypertension (eg, reduced renal mass,40 renal artery banding,40 41 and deoxycorticosterone ...
The latest market report published by Credence Research, Inc. "Global Angiotensin Converting Enzyme (ACE) Inhibitors Market - Growth, Share, Opportunities, Competitive Analysis, and Forecast, 2016 - 2022," the angiotensin converting enzyme (ACE) inhibitors market was valued at USD 11,477.1 Mn in 2015, and is expected to reach USD 11,094.6 Mn by 2023, expanding at a CAGR of (0.5%) from 2016 to 2023.. Browse the full report Angiotensin Converting Enzyme (ACE) Inhibitors Market - Growth, Share, Opportunities, Competitive Analysis, and Forecast, 2016 - 2023 report at http://www.credenceresearch.com/report/angiotensin-converting-enzyme-ace-inhibitors-market. Market Insights. ACE inhibitors are class of drugs (angiotensin-converting enzyme inhibitors) that block the conversion of angiotensin I to angiotensin II, used in the treatment of hypertension and congestive heart failure and in the prevention of microvascular complications of diabetes mellitus. According to World Health Organization (WHO), ...
The compound 4-tert-butyl-2,6-bis(thiomorpholin-4-ylmethyl)phenol (TBTIF) has molecular characteristics similar to angiotensin-converting enzyme (ACE) inhibitors of the sulfhydryl subclass. To assess its value as a new therapeutic agent, we performed
Stroke is the third commonest cause of adult death and the commonest cause of adult disability in the UK. Arterial stiffness is a recognised independent risk factor for cerebrovascular disease. Phase I of the thesis examines arterial stiffness in the context of stroke, evaluating its role as a risk factor and relevance to other abnormalities of cardiovascular regulation during the acute stroke phase. Central, but not peripheral, arterial stiffness was increased in acute ischaemic stroke, particularly in lacunar and atherothrombotic but not cardioembolic subtypes compared to matched controls. Prognostically-important haemodynamic parameters following stroke, for example impaired cardiac baroreceptor sensitivity and increased beat-to-beat blood pressure (BP) variability, were related to central arterial stiffness.;There is uncertainty over the treatment of elevated BP levels following acute stroke. Angiotensin-converting enzyme inhibitors (ACEI) have not been tested in the immediate post-stroke ...
ACE inhibitor use was associated with lower mean grip strength at baseline (22.40 kg, 95% confidence interval (CI) = 21.89-22.91 vs 23.18 kg, 95% CI 23.02-23.34; P = .005) and greater mean annual change in number of chair stands (−0.182, 95% CI −0.217 to −0.147 vs −0.145, 95% CI −0.156 to −0.133; P = .05) than nonuse. Statin use was not significantly associated with baseline measures or mean annual change for any outcome. A subgroup analysis suggested that statin use was associated with less mean annual change in chair stands (P = .006) in the oldest women. ...
Both angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) reduce angiotensin action. Angiotensin, a powerful hormone, has many actions, the most important of which is constriction of small blood vessels, leading to a rise in blood pressure and therefore in the pressure of blood within the glomerular capillaries in the kidneys. Lowering this pressure may well be the mechanism by which these drugs tend to slow progression of kidney failure.. The effects of ACEIs differ from those of ARBs in several important respects. It is even conceivable that taking drugs from both classes is more effective than taking just one or the other alone. Unfortunately, side-to-side comparisons of these two classes of drugs have not been performed, because the drug industry has no interest in such trials. These drugs are also effective in reducing urinary protein excretion in the nephrotic syndrome, and they also slow progression of chronic renal failure even when added to a ...
I recently reviewed a paper that indicated that angiotensin blockade with an angiotensin receptor blocker (ARB) did not protect against the development of diabetic nephropathy in diabetic patients with normal renal function. Despite what that paper concluded angiotensin blockade with and an angiotensin converting enzyme (ACE) inhibitor offered protection.. Two papers in the July 7 Annals of Internal Medicine looked at the effect of ARBs in patients with renal disease. The first study included patients with high vascular risk but who did not have microalbuminuria; about a third were diabetic. In these patients the ARB telmisartan had no effect on major renal outcomes.. The second study was of normotensive diabetic patients. Candesartan (another ARB given at a maximum dose of 32 mg daily) did not prevent microalbuminuria in patients with either type 1 or type 2 diabetes. This makes three studies which indicate no salutary renal effect of ARBs.. The clinician is left wondering if ACE inhibitors are ...
Results of the present study, which was performed in a rat model of CHF, show that both early (7 days after MI) and delayed (3 months after MI) treatments with an ACE inhibitor increase survival and exert beneficial effects on cardiac hemodynamics and remodeling. Moreover, at 9 months after MI, the beneficial effects of the early and late treatments on cardiac hemodynamics (as assessed on the basis of decreased LVEDP and central venous pressure) and on cardiac remodeling (as assessed on the basis of the effect on hypertrophy, ventricular dilatation, and ventricular collagen accumulation) appear to be quantitatively similar. Thus, given the fact that the early treatment was initiated in a setting of moderate ventricular dysfunction and cardiac remodeling, whereas late treatment was initiated in a context of severe LV dysfunction and established remodeling, our experiments suggest that ACE inhibitors are capable of both preventing (in the case of early treatment) and reversing (in the case of late ...
TY - JOUR. T1 - Val-tyr, an Angiotensin I Converting Enzyme Inhibitor from Sardines that have Resistance to Gastrointestinal Proteases. AU - Seki, Eiji. AU - Osajima, Katsuhiro. AU - Matsufuji, Hiroshi. AU - Matsui, Toshiro. AU - Osajima, Yutaka. PY - 1995/1/1. Y1 - 1995/1/1. N2 - The NH2-terminal residue of a dipeptide is an important determinant of the resistance to peptidases of porcine small mucosa. NH2-terminal Val or Ile, and COOH-terminal Trp or Tyr dipeptides had higher angiotensin I converting enzyme(ACE)inhibitory activity and digestive resistance than other dipeptides. We defined Val-Tyr as a main inhibitor in alkaline protease hydrolyzates from sardines. Attempts to isolate and measurement of Val-Tyr were done from the short chain peptides that reduced blood pressure. The content of Val-Tyr was 51 mg per 100 g of the short chain peptides, represented 1.3% of the total ACE inhibitory activity of the short chain peptides. Isolated Val-Tyr was resistant to gastrointestinal proteases. ...
β-Blockers worsen asthma and may mask symptoms of low blood glucose. Therefore, they are not commonly used in people with asthma or diabetes. They can cause fatigue, dizziness, sleep disturbance and nightmares, and various skin disorders. Some people experience cold hands and feet because of decreased blood flow to the limbs. β-Blockers are best used for people who have had a myocardial infarction because they lower the work of the heart. They also are a good agent to use for people who have exercise-induced high blood pressure.. Angiotensin-converting enzyme (ACE) inhibitors block production of a blood pressure-regulating hormone, angiotensin II. Angiotensin II causes constriction, or narrowing, of the arteries that results in elevated blood pressure. Angiotensin-converting enzyme inhibitors allow blood vessels to relax by reducing circulating angiotensin II. This leads to lower blood pressure and improved cardiac output. Angiotensin-converting enzyme inhibitors also protect the kidneys and ...
2,177例の参加者を対象とした4件のRCTが選択基準を満たした。これらのうち、3件はACEiをプラセボと比較し、1件はACEiをARBと比較していた。2件の研究は全体的に低バイアスリスクであり、他の2件のバイアスリスクは中等度から高度と考えられた。質が低~中等度のエビデンス(1,906例の患者を対象とした2件の研究による)では、ステージ3のCKD患者における総死亡(RR 1.80、95%CI 0.17~19.27、P = 0.63)および心血管系イベント(RR 0.87、95%CI 0.66~1.14、P = 0.31)に対しACEiによる影響はないと示唆された。総死亡では、結果にかなりの異質性を認めた。1件の研究(質評価:バイアス低リスク)では、ACEi投与を受けたeGFR , 45 mL/min/1.74 m2の患者において、プラセボに比べて末期腎疾患リスクに差はみられなかった(RR 1.00、95%CI 0.09~1.11、P = ...
The results of this investigation support the hypothesis that higher levels of FGF-23 are associated with cardiovascular mortality and incident heart failure in patients with SIHD. Of note, akin to what has been observed for hs-CRP (25), risk was seen with plasma FGF-23 levels well within the observed range in the general population without known cardiovascular disease or renal impairment (7,15). We also show that FGF-23 provides incremental prognostic information even after adjusting for clinical risk factors, renal function, and cardiovascular biomarkers. Lastly, leveraging data from a randomized controlled trial, we demonstrate that patients with higher levels of FGF-23 received clinical benefit from ACE inhibitor therapy, independent of renal function.. FGF-23 is a phosphatonin that is synthesized and secreted by osteoblasts into the circulation. At normal levels, FGF-23 acts primarily in the kidney to maintain phosphate homeostasis by inducing urinary phosphate excretion (26,27). Elevated ...
The IUPHAR/BPS Guide to Pharmacology. Angiotensin-converting enzyme 2 - M2: Angiotensin-converting (ACE and ACE2). Detailed annotation on the structure, function, physiology, pharmacology and clinical relevance of drug targets.
When first introduced in 1981, angiotensin-converting enzyme (ACE) inhibitors were indicated only for treatment of refractory hypertension. Since then, they have been shown to reduce morbidity or mortality in congestive heart failure, myocardial infarction, diabetes mellitus, chronic renal insufficiency, and atherosclerotic cardiovascular disease. Pathologies underlying these conditions are, in part, attributable to the renin-angiotensin-aldosterone system. Angiotensin II contributes to endothelial dysfunction. altered renal hemodynamics, and vascular and cardiac hypertrophy. ACE inhibitors attenuate these effects. Clinical outcomes of ACE inhibition include decreases in myocardial infarction (fatal and nonfatal), reinfarction, angina, stroke, end-stage renal disease, and morbidity and mortality associated with heart failure. ACE inhibitors are generally well tolerated and have few contraindications. (Am Fam Physician 2002;66:473.)
ACE inhibitors inhibit the hormone angiotensin II responsible for narrowing of blood vessels; thus blood vessel relaxes and lowers blood pressure.
The latest market report published by Credence Research, Inc. "Global Angiotensin Converting Enzyme (ACE) Inhibitors Market - Growth, Share, Opportunities, Competitive Analysis, and Forecast, 2016 - 2022," the angiotensin converting enzyme (ACE) inhibitors market was valued at USD 11,477.1 Mn in 2015, and is expected to reach USD 11,094.6 Mn by 2023, expanding at a CAGR of (0.5%) from 2016 to 2023.. Market Insights. ACE inhibitors are class of drugs (angiotensin-converting enzyme inhibitors) that block the conversion of angiotensin I to angiotensin II, used in the treatment of hypertension and congestive heart failure and in the prevention of microvascular complications of diabetes mellitus. According to World Health Organization (WHO), globally cardiovascular disease accounts for approximately 17 million deaths a year, nearly one third of the total. Of these, complications of hypertension account for 9.4 million deaths worldwide every year ACE inhibitors market is segmented on the basis of ...
Competing interests Dr LP reports grants and personal fees from Sanofi, personal fees from Servier, outside the. submitted work; Dr RR reports grants and personal fees from Sanofi, personal fees from. AstraZeneca, personal fees and non-financial support from Novartis, personal fees from. MSD, outside the submitted work; M. YE has nothing to disclose; Dr MM reports grants. and personal fees from MSD, Novartis, Novo Nordisk, Sanofi and Servier, personal fees and. non-financial support from Abbott, Intarcia, and Eli Lilly, outside the submitted work; Dr. UZ reports personal fees from Astra Zeneca, personal fees from Boehringer Ingelheim,. personal fees from Novartis, personal fees from BMS, personal fees from Sanofi, personal. fees from MSD, personal fees from Pfizer, outside the submitted work; Dr. Reid reports. grants from Sanofi Aventis, during the conduct of the study; Dr MO reports personal fees. from Abbott Vascular, personal fees from Abiomed, personal fees from Astra Zeneca, personal fees ...
ACE inhibitors reduce the production of the enzyme angiotensin, which makes blood vessels constrict. ACE inhibitors allow blood vessels to expand so that blood can flow more easily and the heart can work more efficiently. Examples of commonly prescribed ACE inhibitors are benazepril, captopril, enalapril, lisinopril, and others.. Angiotensin II receptor blockers block the effects of angiotensin, preventing it from affecting the heart and blood vessels. Examples of angiotensin II receptor blockers are candesartan, losartan, telmisartan, valsartan, and others.. Pregnant women should not take ACE inhibitors or ARBs. These medicines can cause a risk of birth defects. If you have high blood pressure and plan to become pregnant or are pregnant, contact your healthcare provider right away.. ...
... (Angiotensin-Converting Enzyme) Inhibitors are drugs used to treat high blood pressure and heart failure. They stop the bodys ability to produce angiotensin II, a natural substance that causes blood vessels to tighten (contract). ACE inhibitors relax and expand (dilate) blood vessels, allowing blood to flow more easily. This increases the supply of blood and oxygen to the heart, making the heart work more easily and efficiently. (Also known as antihypertensive drugs.). ...
ACE inhibitors are medicines used to treat high blood pressure. ACE stands for angiotensin converting enzyme. New research suggests that ACE inhibitors may increase the risk of breast cancer recurrence.. A study found that women treated for early-stage breast cancer were more than 50% more likely to have the cancer come back (recur) if they were taking an ACE inhibitor compared to women who didnt take an ACE inhibitor. The research is published online in Breast Cancer Research and Treatment.. Researchers looked at the health histories of 1,779 women treated for early-stage breast cancer; 23% of the women at some point had taken an ACE inhibitor, a beta-blocker (another type of blood pressure medicine), or both to treat high blood pressure.. During more than 8 years of follow-up after breast cancer was diagnosed and treated, 229 of the women had a recurrence. The researchers compared the risk of recurrence between women treated with blood pressure medicines to women who never took these ...
We started with ACE inhibitor trials in the late 80s and 90s, and when compared to placebo, ACE inhibitors were shown to reduce not only mortality but also MI," lead investigator Sripal Bangalore, MD, New York University School of Medicine, told TCTMD. "In other words, they were shown to have a profound effect. And positive trials tend to have a long-lasting, lingering effect on everybody, including physicians and the guidelines.". ARBs emerged later, he noted, with randomized trials conducted between 2000 to 2010, but these clinical trials did not consistently show a mortality benefit compared with placebo. "This led many people to say, including the guideline writers, that ACE inhibitors are better and should be the frontline treatment," said Bangalore.. In the meta-analysis, published January 2016 in the Mayo Clinic Proceedings, the researchers studied 106 randomized trials that enrolled 254,301 patients without heart failure. Compared with placebo, treatment with an ACE inhibitor ...
Heart failure (HF), the common end stage of most forms of heart disease, afflicted 2.5% of the US population (2.7 million people) in 2006 and was the cause of death for almost 300 000 people in 2005. The National Heart, Lung, and Blood Institute Framingham study has shown that 80% of men and 70% of women with HF under age 65 will die within 8 years.1 The estimated total cost of HF in 2009 is more than $37 billion.2. Clinical Perspective on p 527. By definition, the physiology of the most common form of HF, systolic HF (sHF), always includes an increase in both preload and afterload and a decrease in systolic left ventricular (LV) function. Current therapy for sHF includes diuretics, aldosterone antagonists, angiotensin-converting enzyme inhibitors, angiotensin receptor inhibitors, and β-blockers. Whereas the control of loading conditions, for example, with diuretics and angiotensin-converting enzyme inhibitors, shows clinical benefits,3 improving the inotropic defect of the failing myocardium ...
The renin-angiotensin system (RAS) and angiotensin II, in particular, play a central role and have been implicated in the spectrum of cardiovascular disease (CVD), beginning with hypertension, diabetes mellitus, atherosclerosis, myocardial infarction (MI), strokes and heart failure.
... definition. Explain ACE inhibitor. What is ACE inhibitor? ACE inhibitor meaning. ACE inhibitor sense. ACE inhibitor FAQ. ACE inhibitor synonyms.
Information, Tools, and Resources to aid Primary Care Physicians in caring for Children with Special Health Care Needs (CSHCN) and providing a Medical Home for all of their patients.
Recent studies have revealed significant contributory functions of RAS in the pathophysiology of AD. Activation of RAS in the AD brain was reported by some groups.9-11 These findings support the attractive hypothesis that inhibition of the brain RAS could be a new therapeutic strategy for AD.12 Indeed, a recent study showed that treatment with brain-penetrating ACE inhibitors slowed the rate of cognitive decline in AD patients in comparison with other antihypertensive medication.21 However, some in vitro studies have suggested that ACE could play an important role in the metabolism of Aβ,22,23 demonstrating that ACE degraded Aβ and ACE inhibition increased Aβ levels. On the other hand, as treatment of Tg2576 mice with an ACE inhibitor promoted Aβ deposition,24 treatment with ACE inhibitors might be a risk factor for AD. This effect of ACE inhibition on Aβ metabolism should be carefully considered, especially in relation to long-term treatment with ACE inhibitors. Additional studies are ...
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BACKGROUND: Limited recent data are available describing the patterns of use of angiotensin converting enzyme inhibitor (ACEI) therapy in patients with acute myocardial infarction (AMI), particularly from the more generalizable population-based setting. The purpose of this study was to examine trends in the receipt of ACEIs and associated short-term outcomes in patients hospitalized with AMI in a large Northeastern community. METHODS: We conducted a community-wide study of 7991 patients hospitalized with AMI in all metropolitan Worcester, Massachusetts, medical centers during 8 annual periods between 1990 and 2003. RESULTS: Among all patients, 44% received ACEI therapy during their acute hospitalization. There was a marked increase in the use of ACEIs between 1990 (23%) and 2003 (68%), particularly among those who were not on ACEIs before hospitalization. Patients who were previously on ACEIs were more likely to receive this therapy during hospitalization for AMI than were patients who were not
Why do I need to take ACE inhibitors? ACE inhibitors are used to treat congestive heart failure (CHF) and high blood pressure (hypertension). You may also be given ACE inhibitors after you have had a heart attack , because some studies have shown that these medicines may prevent further damage to the heart muscle.
Angiotensin-converting enzyme inhibitors are a class of medications used in the treatment of hypertension (high blood pressure), congestive heart failure, and other conditions.
Enzyme Inhibitors are substances that reduce the rate of enzyme activity in an enzyme catalysed reaction.These substances may be in the form of molecules or ions that mimic the actual substrates in order to bind to the active site of the enzyme to form an enzyme-inhibitor(EI) complex.Enzyme inhibitors are of two types; 1) Irreversible Inhibitors 2) Reversible Inhibitors Irreversible Inhibitors These substances binds permanently to the active site of an enzyme to form an EI complex.These interraction usually occurs via a strong covalent bond between the enzyme and the inhibitor.It may also occur via a strong non-covalent linkage.In Irreversible inhibition, the separation of the inhibitor from the active site is usually very slow because of the strong covalent linkage that exist between the inhibitor and the enzyme.Irreversible inhibitors are used in Pharmaceuticals for the synthesis of drugs.An example is the inhibition of acetylcholinesterase by Sarin gas which reacts with the hydroxyl group of ...
ACE inhibitors, also called angiotensin-converting enzyme inhibitors, are drugs used to treat high blood pressure and heart failure. ACE inhibitors s alters the bodys ability to produce angiotensin II, a hormone that causes the arteries to narrow. By blocking the making of angiotensin, these drugs help the blood vessels relax and widen, which lowers blood pressure, increases blood flow to the heart and reduces the hearts workload. ...
Angiotensin-converting enzyme (ACE) inhibitor-diuretic combinations help treat high blood pressure. Learn more about ACE from Discovery Health.
More than 3 decades ago, the landscape of cardiovascular preventive care started to change. The Veterans Administration Cooperative Study (1) provided the first definitive evidence that antihypertensive drugs were efficacious in preventing major cardiovascular events. Since then, other classes of drugs for other risk factors have been tested and found to be valuable for preventing the occurrence or delaying progress of a wide variety of vascular diseases. Thus, β-blockers, aspirin, and angiotensin-converting enzyme inhibitors are now standard in the armamentarium of cardiovascular preventive care. A massive database has substantiated the value of lipid-lowering therapy in primary and secondary prevention since 1994. The most recent primary prevention trial, the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) (2), shows the value of treating healthy persons who have abnormal blood lipid levels. The question that must be answered for the practice of preventive ...
in New England Journal of Medicine [=NEJM] (2011), 364. BACKGROUND: Microalbuminuria is an early predictor of diabetic nephropathy and premature cardiovascular disease. We investigated whether treatment with an angiotensin-receptor blocker (ARB) would delay or ... [more ▼]. BACKGROUND: Microalbuminuria is an early predictor of diabetic nephropathy and premature cardiovascular disease. We investigated whether treatment with an angiotensin-receptor blocker (ARB) would delay or prevent the occurrence of microalbuminuria in patients with type 2 diabetes and normoalbuminuria. METHODS: In a randomized, double-blind, multicenter, controlled trial, we assigned 4447 patients with type 2 diabetes to receive olmesartan (at a dose of 40 mg once daily) or placebo for a median of 3.2 years. Additional antihypertensive drugs (except angiotensin-converting-enzyme inhibitors or ARBs) were used as needed to lower blood pressure to less than 130/80 mm Hg. The primary outcome was the time to the first onset of ...
Large clinical trials have shown that inhibition of the renin-angiotensin system (RAS) can delay and/or prevent the onset of Type 2 diabetes mellitus (T2DM) in high-risk individuals, such as those with hypertension or chronic heart failure. Moreover, a meta-analysis of these randomized clinical studies concluded that the mean weighted relative risk of development of T2DM was reduced by 25% in those patients treated with angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors. In spite of these firm clinical data, the mechanistic pathways mediating the protective activity of RAS blockade have yet to be resolved ...
Auro-Valsartan: Valsartan belongs to a family of medications known as angiotensin II receptor blockers. These medications are used to lower mild-to-moderate high blood pressure. Valsartan is also used to treat chronic heart failure or to reduce the risk of death after a heart attack in people who cannot use another type of medication called angiotensin-converting enzyme inhibitor.
A growing body of evidence supports the notion that angiotensin II (Ang II), the central product of the renin-angiotensin system, may play a central role not only in the etiology of hypertension but also in the pathophysiology of cardiovascular and renal diseases in humans. In this review, we focus on the role of Ang II in cardiovascular and renal diseases at the molecular and cellular levels and discuss up-to-date evidence concerning the in vitro and in vivo actions of Ang II and the pharmacological effects of angiotensin receptor antagonists in comparison with angiotensin-converting enzyme inhibitors. Ang II, via AT1 receptor, directly causes cellular phenotypic changes and cell growth, regulates the gene expression of various bioactive substances (vasoactive hormones, growth factors, extracellular matrix components, cytokines, etc.), and activates multiple intracellular signaling cascades (mitogen-activated protein kinase cascades, tyrosine kinases, various transcription factors, etc.) in ...
Enzyme Inhibitors and Activators. By Olga D. Lopina. Enzymes are very effective biological catalysts that accelerate almost all metabolic reactions in living organisms. Enzyme inhibitors and activators that modulate the velocity of enzymatic reactions play an important role in the regulation of metabolism. Enzyme inhibitors are also useful tool for study of enzymatic reaction as well as for design of new medicine drugs. In this chapter, we focused on the properties of enzyme inhibitors and activators. Here we present canonical inhibitor classification based on their kinetic behavior and mechanism of action. We also considered enzyme inhibitors that were used for design of various types of pharmacological drugs and natural inhibitors as a plausible source for design of future drugs. Mechanisms of action of enzyme activators and some features of allosteric modulators are considered.. Part of the book: Enzyme Inhibitors and Activators ...
Angiotensin Converting Enzyme (ACE), a metallo-peptidase is the best known important drug target in the treatment of hypertension and responds to broad range ACE inhibitors such as Captopril. Whilst, many phytochemical compounds including alkaloids and flavonoids were also reported with anti-hypertensive activity. On the other hand, ACE2 is considered as an interesting new cardio-renal disease target as it is close and unique ACE homologue. In this scenario, the anti-hypertensive activities of 17 phytochemical compounds were analyzed through docking studies with ACE2. Also, the other ACE inhibitors with reported IC50 values were considered for docking interactions and used as training set. Further, the best docked phytochemical compound Rosemarinic acid and the training set compounds with ACE inhibitor activity were used to design the pharmacophore and validated. The generated 3D pharmacophore is subjected to screen the compounds with the significant chemical features against May bridged database
www.MOLUNA.de Cardiac Drug Therapy [4259362] - 1. Beta-Blockers: The Cornerstone of Cardiac Drug Therapynn2. Beta-Blocker Controversiesnn3. Angiotensin-Converting Enzyme Inhibitors and Angiotensin II Receptor Blockersnn4. ACE Inhibitor Controversiesnn5. Calcium Antagonists (Calcium Channel Blockers)nn6. Calcium Antagonist Controversiesnn7. Diureticsnn8. Hypertensionnn9. Hypertension Controversiesnn10. Anginann11. Acute Myocardial Infarctionnn12. Heart Failurenn13. Heart Failure Controversiesnn14. Management of Cardiac Arrhythmiasnn15. Cardiac Arrestnn16. Management of
MONDAY, Jan. 4, 2016 (HealthDay News) -- Newer blood pressure drugs are as safe and effective as older medications, new research suggests.. Scientists at the NYU Langone Medical Center in New York City said their findings settle a longstanding debate about which of two types blood-pressure lowering medications studied are better.. An analysis of 106 randomized trials involving more than 250,000 patients examined the effects of newer angiotensin receptor blockers (ARBs) and older angiotensin-converting enzyme (ACE) inhibitors. Although ACE inhibitors were developed 10 years earlier, both types of drugs showed similar effects in the analysis, challenging previous findings that suggest ACE inhibitors have greater benefits.. According to the new analysis, published online Jan. 4 in the Mayo Clinic Proceedings, the only difference between the medications is that ARBs are more easily tolerated.. "There has been debate for many years over the safety and efficacy of ACE inhibitors compared to ARBs, with ...
Many drugs used in cardiovascular therapy have antiinflammatory properties in addition to their targeting actions on modifying risk factors, such as hypertension and hyperlipidaemia [105]. Among them, ACEIs (angiotensin-converting enzyme inhibitors), ARBs (angiotensin II type 1 receptor blockers), calcium channel blockers, the antiplatelet agent clopidogrel, and PPAR (peroxisome-proliferator-activated receptor)-α and PPAR-γ activators appear to be involved in inflammatory pathways, but the clinical benefits of these effects remain unclear in cardiovascular diseases. In the same manner, atheroprotective action of statins, mainly used for their cholesterol-lowering effect, could also be attributed to their antiinflammatory properties [106-109].. At the present time, great efforts are engaged in identifying novel and innovative drugs targeting inflammatory proteins for the treatment of atherosclerosis. Potential inflammatory targets are factors involved in the recruitment of leucocytes, including ...
The guidelines above are for the general population, but seniors health needs and benchmarks differ from those of younger individuals in many ways. While 130/80 mmHg is the generic threshold for beginning BP medications, there have been many disagreements among medical professionals regarding the threshold for older adults. Age, frailty and other comorbidities like diabetes and chronic kidney disease complicate this matter even further.. The Eighth Joint National Committee (JNC 8) issued guidelines in 2013 recommending that individuals over age 60 aim for a reading below 150/90 mmHg. The JNC 8 recommendation for patients of any age with diabetes or chronic kidney disease is to aim for BP readings below 140/90 mmHg. These are not hard and fast rules, though, because each seniors health needs are unique.. "The JNC 8 guidelines support what we geriatricians have believed for quite some time: many older adults are taking too much BP medication," says Dr. Leslie Kernisan, M.D., M.P.H. In addition ...
ACE Inhibitors NCLEX questions for nursing students! ACE Inhibitors are medications used to help lower the blood pressure. The nurse should be aware of how the drug works, why it is ordered, nursing implications, adverse reactions, and how to teach the patient how to take the medication.
http://sageke.sciencemag.org/cgi/content/abstract/sageke;2002/11/nw35 Abstract: B. Onder, B. W. J. H. Penninx, R. Balkrishnan, L. P. Fried, P. H. M. Chaves, J. Williamson, C. Carter, M. Di Bari, J. M. Guralnik, M. Pahor, Relation between use of angiotensin-converting enzyme inhibitors and muscle strength and physical function in older women: an observational study. Lancet 359, 926-930 (2002). [Abstract] [Full Text]. Citation: Another Noteworthy Paper This Week (20 March 2002). Sciences SAGE KE (20 March 2002), http://sageke.sciencemag.org/cgi/content/abstract/sageke;2002/11/nw35 ...
آنزیم ۲ مبدل آنژیوتانسین (به انگلیسی: Angiotensin-converting enzyme 2) یا به اختصار ACE2، یک اگزوپپتیداز است که موجب تبدیل آنژیوتانسین ۱ به «آنژیوتانسین ۹-۱» (نُه پپتیدی)،[۳] یا تبدیل آنژیوتانسین ۲ به «آنژیوتانسین ۷-۱» می‌گردد.[۴][۵] این آنزیم اثرات مستقیمی بر عملکرد قلب دارد،a و بیشتر در لایهٔ داخلی رگ‌های خونی، قلب و کلیه‌ها بیان می‌شود.[۶] داروهای بازدارندهٔ آنزیم مبدل آنژیوتانسین که در درمان فشار خون بالا استفاده می‌شوند، اثری بر آنزیم ACE2 ندارند.[۷] مشخص شده که گیرنده‌های ACE2، نقطهٔ ورود برخی از انواع کروناویروس‌ها به سلول‌های بدن انسان هستند.[۸] دو گروه مجزا از ...
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies. ...
Heterogeneous toroidal-spiral particles (TSPs) were generated by polymer droplet sedimentation interaction and cross-linking. released from your dense polymer matrix of poly(ethylene glycol) diacrylate (MW ~ 700 g/mol; PEGDA 700). Released irinotecan inhibited the proliferation of U251 malignant glioma cells. Since the restorative compounds are released through different pathways specifically diffusion through the polymer matrix versus TS channels the release rate can be controlled individually through the design of the structure and material of particle parts. Intro Treatment of complex diseases often requires the simultaneous delivery of multiple restorative providers at optimum administration rates for any synergistic effect.1 The goal of developing vehicles to codeliver multiple therapeutic agents is definitely a significant driver of research.2?4 Manipulating the release of multiple therapeutic providers independently of one another is beneficial for drug synergy. However this can CD7 be ...
Your patient is at least 55 years old, has claims evidence for diabetes, has an additional cardiovascular disease risk factor (eg, history of cardiovascular disease, dyslipidemia, microalbuminuria), and has no claims evidence for an angiotensin-converting enzyme (ACE) inhibitor. The American Diabetes Association recommends that, in these patients, with or without hypertension, an ACE inhibitor be considered to reduce the risk of cardiovascular events. If your patient fits this clinical profile, and if not already done or contraindicated, consider starting an ACE inhibitor and titrating the dosage as tolerated ...
Angiotensin-Converting Enzyme (ACE) Inhibitor or Angiotensin Receptor Blocker (ARB) Therapy - for patients with CAD and Diabetes or Left Ventricular Systolic Dysfunction (LVEF,40%) ...
Angiotensin-Converting Enzyme (ACE) Inhibitor or Angiotensin Receptor Blocker (ARB) Therapy - for patients with CAD and Diabetes or Left Ventricular Systolic Dysfunction (LVEF , 40 ...
ACE inhibitors have side effects just like any other drugs. It can feel as if you have a bad cold because many of the symptoms that are possible are a cough, sore throat, fever, and mouth sores. Other symptoms include an itchy, red skin rash, swelling of the neck, face or tongue, or a salty or metallic taste in your mouth. While all of these are not extremely common, they have been reported in enough cases to be listed as possible side effects to taking ACE inhibitors ...
Angoitensin Converting Enzyme inhibitors are commonly prescribed for hypertension. The generic names designated for ACE inhibitors usually end in the
Title: MedicineNet ACE Inhibitors Specialty, Description: MedicineNet ACE Inhibitors Specialty, By: Feedage Forager, ID: 330972, Grade: 89, Type: RSS20
Angiotensin-Converting Enzyme (ACE) inhibitors and Angiotensin Receptor Blockers (ARBs) alone or in combination have similar effects on cardiovascular and renal outcomes in patients with...
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Administration of an ACE inhibitor can limit the damage caused to heart and lungs by radiotherapy treatment of tumours in the chest region, say researchers.
Current Enzyme Inhibition aims to publish original research, review and letter articles in all the latest and outstanding developments on enzyme inhibition studies. The coverage includes the mechanisms of inhibitory processes of enzymes, recognition of active sites, and the discovery of agonists and antagonists, leading to the design and development of new drugs of significant therapeutic value.
Current Enzyme Inhibition aims to publish original research, review and letter articles in all the latest and outstanding developments on enzyme in...
A compilation of questions the Anticancer Fund has received from patients or their relatives. All of these answers have been carefully written by professionals of our team for informational purpose only ...
Looking for online definition of Angiotensin-converting enzyme inhibitor in the Medical Dictionary? Angiotensin-converting enzyme inhibitor explanation free. What is Angiotensin-converting enzyme inhibitor? Meaning of Angiotensin-converting enzyme inhibitor medical term. What does Angiotensin-converting enzyme inhibitor mean?
Cardiovascular diseases are a major cause of death in Western countries. Angiotensin-converting enzyme (ACE) is as a key enzyme in the renin-angiotensin system involved in the regulation of blood pressure, and water and electrolyte balance in the body. ACE not ouly increases the conversion of angiotensin I to the active angiotensin II, but also degrades bradykinin. ACE inhibitors, like captopril, are today first-line treatment in hypertension and heart failure.. We have shown that two structurally different ACE inhibitors, captopril and fosinopril, exhibit anti-atherosclerotic effects in hypercholesterolemic mini pigs. Captopril, but not fosinopril, improved endothelial function in the iliac arteries from the mini pigs.. Bradykinin-induced relaxation of porcine iliac arteries was mediated by bradykinin B2 receptors and the subsequent release of nitric oxide (NO). ACE inhibitors did not affect the bradykinin-induced relaxation, implying that other enzymes than ACE (e. g. carboxypeptidase M; CPM) ...
China Pharmaceutical Powder Orally Active Ace Inhibitor Lisinopril, Find details about China Lisinopril, Pharmaceutical Chemical from Pharmaceutical Powder Orally Active Ace Inhibitor Lisinopril - Wuhan Dahua Weiye Pharmaceutical Chemical Co., Ltd.
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 ...
People who take ACE inhibitors may develop angioedema, a condition that causes itchy and painful swelling beneath the skin around the eyes, lips, tongue, throat, hands, or feet. In severe cases, the throat may swell, obstructing the airway and leading to breathing difficulty. ACE inhibitors prevent the breakdown of a natural chemical in the body called bradykinin. Increased levels of bradykinin, which can cause swelling, may contribute to the development of angioedema. Blocking bradykinin receptor cells prevents bradykinin from initiating swelling and may lead to a possible decrease in angioedema symptoms. The purpose of this study is to evaluate the effectiveness of HOE-140, a bradykinin receptor blocker, at reducing symptoms in people with ACE inhibitor-associated angioedema.. This study will enroll people admitted to the emergency room or hospital who have a severe case of ACE inhibitor-associated angioedema. Participants will be randomly assigned to receive an injection of either HOE-140 or ...
The leukocyte migration induced by Phoneutria nigriventer spider venom (PNV) has been investigated in rats using the pleurisy model. Intrapleural injection of PNV (10-100 mug/cavity) caused a dose- and time-dependent leukocyte accumulation. the bradykinin B-2 receptor antagonist Hoe 140 (0.5 mg/kg) substantially inhibited PNV-induced cell accumulation, whereas the angiotensin-converting enzyme inhibitor captopril (2 mg/kg) potentiated by 80% this effect. the non-specific kallikrein inhibitor aprotinin and the plasma kallikrein inhibitor soybean trypsin inhibitor greatly reduced PNV-induced leukocyte migration, whereas the selective tissue kallikrein inhibitor P-ac-F-S-R-EDDnp failed to affect PNV-induced responses. Treatment of rats with capsaicin (50 mg/kg) at the neonatal stage resulted in 67% inhibition of the PNV-induced cell migration. the neurokinin NK1 receptor antagonist SR140333, but not the NK2 receptor antagonist SR48968, reduced by 55% venom-induced cell accumulation. We conclude ...
Progressive deterioration of renal function occurs during normal aging. Previous studies on the aging kidney have demonstrated glomerular hemodynamic changes, specifically, glomerular capillary hypertension, as maladaptations that lead to proteinuria and glomerular sclerosis over time. Aging rats treated with angiotensin-converting enzyme inhibition have relatively less proteinuria and sclerosis, suggesting that age-related changes in renal function may be associated with alterations in the intrarenal renin-angiotensin system, which thus may play a major role in the pathogenesis of these maladaptations. To investigate this possibility, renal and systemic renin-angiotensin systems were examined at an early phase of the aging process (3 months) and at a later phase (12 months) in male Sprague-Dawley rats. Although plasma renin and serum angiotensin-converting enzyme concentrations did not differ significantly, the intrarenal system showed down-regulation of renin mRNA and angiotensin-converting ...
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 ...
TY - JOUR. T1 - Modeling sex differences in the renin angiotensin system and the efficacy of antihypertensive therapies. AU - Leete, Jessica. AU - Gurley, Susan. AU - Layton, Anita T.. PY - 2018/4/6. Y1 - 2018/4/6. N2 - The renin angiotensin system is a major regulator of blood pressure and a target for many anti-hypertensive therapies; yet the efficacy of these treatments varies between the sexes. We use published data for systemic RAS hormones to build separate models for four groups of rats: male normotensive, male hypertensive, female normotensive, and female hypertensive rats. We found that plasma renin activity, angiotensinogen production rate, angiotensin converting enzyme activity, and neutral endopeptidase activity differ significantly among the four groups of rats. Model results indicate that angiotensin converting enzyme inhibitors and angiotensin receptor blockers induce similar percentage decreases in angiotensin I and II between groups, but substantially different absolute ...

Angiotensin converting enzyme inhibitors in pregnancy.  - PubMed - NCBIAngiotensin converting enzyme inhibitors in pregnancy. - PubMed - NCBI

Angiotensin converting enzyme inhibitors in pregnancy.. Mastrobattista JM1.. Author information. 1. Department of Obstetrics, ... Angiotensin converting enzyme (ACE) inhibitors are excellent antihypertensive agents and are becoming widely used as first-line ... Angiotensin-Converting Enzyme Inhibitors/adverse effects. *Angiotensin-Converting Enzyme Inhibitors/therapeutic use* ... This review discusses the mechanism of action of ACE inhibitors and the use of ACE inhibitors in pregnancy both in experimental ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/9201818?dopt=Abstract

Angiotensin-Converting Enzyme Inhibitors | GreenMedInfoAngiotensin-Converting Enzyme Inhibitors | GreenMedInfo

Pharmacological Actions : Alpha-amylase inhibitor, Alpha-glucosidase inhibitor , Angiotensin-Converting Enzyme Inhibitors, ... Pharmacological Actions : Alpha-amylase inhibitor, Alpha-glucosidase inhibitor , Angiotensin-Converting Enzyme Inhibitors, ... Pharmacological Actions : Angiotensin-Converting Enzyme Inhibitors, Hypotensive, Vascular smooth muscle cell (VSMC) inhibitor ... Pharmacological Actions : Angiotensin-Converting Enzyme Inhibitors, Anti-Angiogenic, Hypotensive, NF-kappaB Inhibitor ...
more infohttp://www.greenmedinfo.com/pharmacological-action/angiotensin-converting-enzyme-inhibitors

DailyMed - Search Results for Angiotensin-converting Enzyme InhibitorsDailyMed - Search Results for Angiotensin-converting Enzyme Inhibitors

SEARCH RESULTS for: Angiotensin-converting Enzyme Inhibitors [Drug Class] (839 results) * Share : JavaScript needed for Sharing ...
more infohttps://dailymed.nlm.nih.gov/dailymed/search.cfm?query=Angiotensin-converting%20Enzyme%20Inhibitors&searchdb=class

Angiotensin-converting enzyme inhibitors--when to use?Angiotensin-converting enzyme inhibitors--when to use?

Although there are theoretical reasons suggesting that ACE inhibitors might be useful in all patients with heart f ... Angiotensin-Converting Enzyme Inhibitors / adverse effects, therapeutic use*. Heart Failure / drug therapy*. Hemodynamics / ... In practice, angiotensin-converting enzyme inhibitors have been shown to given considerable relief to patients with severe ... but the effect is not specific to angiotensin-converting enzyme inhibitors.. ...
more infohttp://www.biomedsearch.com/nih/Angiotensin-converting-enzyme-inhibitors-when/3069209.html

Brief review: Angiotensin converting enzyme inhibitors and angioedema: anesthetic implications | SpringerLinkBrief review: Angiotensin converting enzyme inhibitors and angioedema: anesthetic implications | SpringerLink

Purpose Angiotensin converting enzyme inhibitors (ACEIs) are a group of drugs used to treat hypertension and heart failure, ... Effects of angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists on mortality and renal outcomes in ... Unmasking of acquired autoimmune C1-inhibitor deficiency by an angiotensin-converting enzyme inhibitor. Ann Allergy Asthma ... Angiotensin-converting enzyme (ACE) inhibitors and angio-oedema. Br J Dermatol 1997, 136:153-8.PubMedCrossRefGoogle Scholar ...
more infohttps://link.springer.com/article/10.1007%2FBF03022528

Angiotensin Converting Enzyme Inhibitors in Cardiovascular Disease (Expert ConseAngiotensin Converting Enzyme Inhibitors in Cardiovascular Disease (Expert Conse

... nsus Document on) ESC Clinical Practice ... Effects of ACE-inhibitors: Haemodynamic effects, Neurohormonal effects, Antiproliferative effects, Renal effects, Other effects ... Heart failure: Target dose, ACE-I compared with angiotensin, receptor blockers. *Asymptomatic left ventricular systolic ...
more infohttps://www.escardio.org/Guidelines/Clinical-Practice-Guidelines/Angiotensin-Converting-Enzyme-Inhibitors-in-Cardiovascular-Disease-Expert-Conse

Angiotensin-Converting Enzyme Inhibitors for Stroke Prevention | StrokeAngiotensin-Converting Enzyme Inhibitors for Stroke Prevention | Stroke

Angiotensin-Converting Enzyme Inhibitors for Stroke Prevention. Is There HOPE for PROGRESS After LIFE?. Graeme J. Hankey ... Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Engl J Med. ... Lonn EM, Yusuf S, Jha P, Montague TH, Teo KK, Benedict CR, Pitt B. Emerging role of angiotensin-converting enzyme inhibitors in ... Effects of long-term treatment with angiotensin-converting-enzyme inhibitors in the presence or absence of aspirin: a ...
more infohttp://stroke.ahajournals.org/content/34/2/354.full

Angioedema Incidence in US Veterans Initiating Angiotensin-Converting Enzyme Inhibitors | HypertensionAngioedema Incidence in US Veterans Initiating Angiotensin-Converting Enzyme Inhibitors | Hypertension

Renin-Angiotensin System. Angioedema Incidence in US Veterans Initiating Angiotensin-Converting Enzyme Inhibitors. Donald R. ... Effects of angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists on mortality and renal outcomes in ... effect of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Amer Heart J. 2004; 148: 747-754. ... Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Engl J Med. ...
more infohttp://hyper.ahajournals.org/content/51/6/1624

Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors) | Memorial HospitalAngiotensin-Converting Enzyme Inhibitors (ACE Inhibitors) | Memorial Hospital

ACE Inhibitors) at Memorial Hospital Arginine -Possible Harmful Interaction ... ... Angiotensin-converting enzyme inhibitors (ACE inhibitors) block the conversion of a naturally occurring substance, angiotensin ... Severe hyperkalemia during very-low-calorie diets and angiotensin converting enzyme use. JAMA. 1990;264:2737-2738. ... ACE inhibitors may cause zinc depletion. 11,12 The ACE inhibitors captopril and enalapril attach to the trace mineral zinc. ...
more infohttps://memorialhospitaljax.com/hl/?/21382/Accupril&com.dotmarketing.htmlpage.language=1

Bronchial hyperreactivity in patients who cough after receiving angiotensin converting enzyme inhibitors | The BMJBronchial hyperreactivity in patients who cough after receiving angiotensin converting enzyme inhibitors | The BMJ

Angiotensin converting enzyme inhibitors cause cough in some patients, but the mechanism of this effect is not known. Six ... Nine patients in whom angiotensin converting enzyme inhibitors had not been associated with cough served as controls. In the ... Bronchial hyperreactivity in patients who cough after receiving angiotensin converting enzyme inhibitors Br Med J (Clin Res Ed ... Bronchial hyperreactivity in patients who cough after receiving angiotensin converting enzyme inhibitors. Br Med J (Clin Res Ed ...
more infohttp://www.bmj.com/content/296/6615/86

Angiotensin converting enzyme inhibitor-induced renal dysfunction in atherosclerotic renovascular disease.  - PubMed - NCBIAngiotensin converting enzyme inhibitor-induced renal dysfunction in atherosclerotic renovascular disease. - PubMed - NCBI

Angiotensin converting enzyme inhibitor-induced renal dysfunction in atherosclerotic renovascular disease.. van de Ven PJ1, ... Angiotensin converting enzyme inhibition (ACEi) may impair renal function in such patients, but a prospective study of its ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/9551408?dopt=Abstract

Three Candidate Genes and Angiotensin-Converting Enzyme Inhibitor-Related Cough | HypertensionThree Candidate Genes and Angiotensin-Converting Enzyme Inhibitor-Related Cough | Hypertension

Association between cough and angiotensin-converting enzyme inhibitors versus angiotensin II antagonists: the design of a ... Three Candidate Genes and Angiotensin-Converting Enzyme Inhibitor-Related Cough. A Pharmacogenetic Analysis. Robert Y. L. Zee, ... Three Candidate Genes and Angiotensin-Converting Enzyme Inhibitor-Related Cough. Robert Y. L. Zee, Valluri S. Rao, Robert Z. ... Three Candidate Genes and Angiotensin-Converting Enzyme Inhibitor-Related Cough. Robert Y. L. Zee, Valluri S. Rao, Robert Z. ...
more infohttp://hyper.ahajournals.org/content/31/4/925

Medical Subject Headings - Angiotensin-Converting Enzyme Inhibitors - Classes | NCBO BioPortalMedical Subject Headings - Angiotensin-Converting Enzyme Inhibitors - Classes | NCBO BioPortal

Antagonists, Angiotensin Converting Enzyme. Angiotensin I-Converting Enzyme Inhibitors. Angiotensin Converting Enzyme ... Antagonists, Angiotensin-Converting Enzyme. Enzyme Inhibitors, Angiotensin-Converting. Enzyme Antagonists, Angiotensin- ... use TEPROTIDE to search ANGIOTENSIN I-CONVERTING ENZYME INHIBITOR 1991-93. prefLabel. Angiotensin-Converting Enzyme Inhibitors ... Angiotensin-Converting Enzyme. Inhibitors, Angiotensin Converting Enzyme. Kininase II Inhibitors. Angiotensin-Converting Enzyme ...
more infohttp://bioportal.bioontology.org/ontologies/MESH?p=classes&conceptid=http%3A%2F%2Fpurl.bioontology.org%2Fontology%2FMESH%2FD000806

Angiotensin-Converting Enzyme Inhibitors and Chyluria | Annals of Internal Medicine | American College of PhysiciansAngiotensin-Converting Enzyme Inhibitors and Chyluria | Annals of Internal Medicine | American College of Physicians

... showing improvement of lipid abnormalities associated with proteinuria using the Angiotensin-converting enzyme (ACE) inhibitor ... Angiotensin-Converting Enzyme Inhibitors and Chyluria. Ann Intern Med. 1993;119:1223-1224. doi: https://doi.org/10.7326/0003- ...
more infohttps://annals.org/aim/article-abstract/706960/angiotensin-converting-enzyme-inhibitors-chyluria

Angiotensin Converting-Enzyme Inhibitors and the Kidney - WSAVA2007 - VINAngiotensin Converting-Enzyme Inhibitors and the Kidney - WSAVA2007 - VIN

Effect of the angiotensin-converting enzyme-inhibitor benazepril on the progression of chronic renal failure. New Eng J Med ... Long-term follow-up of acute renal failure caused by angiotensin converting enzyme inhibitors. Amer J Hypertens 1998; 11:1080- ... Angiotensin Converting-Enzyme Inhibitors and the Kidney World Small Animal Veterinary Association World Congress Proceedings, ... Potential adverse effects of angiotensin-converting enzyme inhibitors in the treatment of congestive heart failure. Compend ...
more infohttps://www.vin.com/apputil/content/defaultadv1.aspx?pId=11242&meta=Generic&catId=31916&id=3860733&ind=138&objTypeID=17

Isolated unilateral tongue oedema: the adverse effect of angiotensin converting enzyme inhibitors.Isolated unilateral tongue oedema: the adverse effect of angiotensin converting enzyme inhibitors.

Angiotensin converting enzyme inhibitors (ACEI) are widely used to treat benign hypertension. These drugs are generally well ... Angiotensin converting enzyme inhibitors (ACEI) are widely used to treat benign hypertension. These drugs are generally well ... inhibitor, who attended Emergency department with angio-oedema only on the left side of her tongue. Her airway was patent and ...
more infohttp://www.biomedsearch.com/nih/Isolated-unilateral-tongue-oedema-adverse/23320432.html

Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors) | Sky Ridge Medical CenterAngiotensin-Converting Enzyme Inhibitors (ACE Inhibitors) | Sky Ridge Medical Center

ACE Inhibitors) at Sky Ridge Medical Center Arginine -Possible Harmful Interaction ... ... Angiotensin-converting enzyme inhibitors (ACE inhibitors) block the conversion of a naturally occurring substance, angiotensin ... Severe hyperkalemia during very-low-calorie diets and angiotensin converting enzyme use. JAMA. 1990;264:2737-2738. ... ACE inhibitors may cause zinc depletion. 11,12 The ACE inhibitors captopril and enalapril attach to the trace mineral zinc. ...
more infohttps://skyridgemedcenter.com/hl/?/21382/Univasc

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in high vascular risk | HeartAngiotensin-converting enzyme inhibitors and angiotensin receptor blockers in high vascular risk | Heart

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in high vascular risk ... Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in high vascular risk ... Angiotensin-converting enzyme inhibitors versus receptor blockers: is one better than the other for cardiovascular prevention? ... Objective ACE inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are widely prescribed in patients with high ...
more infohttps://heart.bmj.com/content/103/17/1339.abstract

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in high vascular risk | HeartAngiotensin-converting enzyme inhibitors and angiotensin receptor blockers in high vascular risk | Heart

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in high vascular risk ... Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in high vascular risk ... Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in high vascular risk ...
more infohttps://heart.bmj.com/content/103/17/1339.citation-tools

Huntingtons disease: deterioration in clinical state during treatment with angiotensin converting enzyme inhibitor. | The BMJHuntington's disease: deterioration in clinical state during treatment with angiotensin converting enzyme inhibitor. | The BMJ

Huntingtons disease: deterioration in clinical state during treatment with angiotensin converting enzyme inhibitor. Br Med J ( ... Huntingtons disease: deterioration in clinical state during treatment with angiotensin converting enzyme inhibitor.. Br Med J ... Huntingtons disease: deterioration in clinical state during treatment with angiotensin converting enzyme inhibitor. ... Huntingtons disease: deterioration in clinical state during treatment with angiotensin converting enzyme inhibitor. ...
more infohttp://www.bmj.com/content/294/6588/1659.2

The Hospital for Sick Children - Taking angiotensin-converting enzyme inhibitors during pregnancy - Is it safe?The Hospital for Sick Children - Taking angiotensin-converting enzyme inhibitors during pregnancy - Is it safe?

Pregnancy outcome after in utero exposure to angiotensin converting enzyme inhibitors or angiotensin receptor blockers. Reprod ... Fetopathy associated with exposure to angiotensin converting enzyme inhibitors and angiotensin receptor antagonists. Early Hum ... Taking angiotensin-converting enzyme inhibitors during pregnancy - Is it safe?. Almundher Al-Maawali, MD, Asnat Walfisch, MD ... Angiotensin-converting enzyme (ACE) inhibitors are widely used as first-line therapy for chronic hypertension. They are ...
more infohttp://www.motherisk.org/prof/updatesDetail.jsp?content_id=969

angiotensin converting enzyme inhibitors Archives - Ferrer, Poirot & Wansbrough | Drug Injury Lawyers	angiotensin converting enzyme inhibitors Archives - Ferrer, Poirot & Wansbrough | Drug Injury Lawyers

Search Results: angiotensin converting enzyme inhibitors. Blood pressure drug combo could lead to serious drug injuries March ...
more infohttps://www.lawyerworks.com/tag/angiotensin-converting-enzyme-inhibitors/

Residual Renal Function in Hemodialysis Patients: The Role of Angiotensin-Converting Enzyme Inhibitor in Its PreservationResidual Renal Function in Hemodialysis Patients: The Role of Angiotensin-Converting Enzyme Inhibitor in Its Preservation

"Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in peritoneal dialysis: systematic review and meta- ... The effect of angiotensin-converting enzyme inhibitor (ACEi) on reducing the rate of decline of GFR in proteinuric ... The role of angiotensin-converting enzyme inhibitor (ACEi) in preserving renal function in chronic proteinuric nephropathies is ... G. Maschio, D. Alberti, G. Janin et al., "Effect of the angiotensin-converting-enzyme inhibitor benazepril on the progression ...
more infohttps://www.hindawi.com/journals/isrn/2013/184527/

Residual Renal Function in Hemodialysis Patients: The Role of Angiotensin-Converting Enzyme Inhibitor in Its PreservationResidual Renal Function in Hemodialysis Patients: The Role of Angiotensin-Converting Enzyme Inhibitor in Its Preservation

The role of angiotensin-converting enzyme inhibitor (ACEi) in preserving renal function in chronic proteinuric nephropathies is ... Residual Renal Function in Hemodialysis Patients: The Role of Angiotensin-Converting Enzyme Inhibitor in Its Preservation. ...
more infohttps://www.hindawi.com/journals/isrn/2013/184527/abs/
  • The results of the HOPE and LIFE trials, and to a lesser extent SCOPE, indicate that inhibiting the formation or action of angiotensin II prevents stroke and other vascular events (and perhaps new-onset diabetes) and suggest that a substantial proportion of the effect may be independent of BP lowering. (ahajournals.org)
  • It was the first ACE inhibitor developed and was considered a breakthrough both because of its novel mechanism of action and also because of the revolutionary development process. (wikipedia.org)
  • Most published studies have failed to show an effect of ACE inhibitors on congenital malformations. (motherisk.org)
  • Cooper and colleagues 9 reported an increased risk of congenital malformations in fetuses exposed to ACE inhibitors during the first trimester. (motherisk.org)
  • BestBets: Should angiotensin converting enzyme inhibitors be used in children with Type 1 diabetes and microalbuminuria? (bestbets.org)
  • ACE inhibitors have been shown to reduce heart failure-related hospitalisations, prolong life, and improve exercise tolerance and quality of life. (heartfailurematters.org)
  • While the results of animal studies on the use of ACE inhibitors during pregnancy vary, most of them have failed to show increased malformation rates. (motherisk.org)
  • The authors report a 64-year-old Caucasian woman with a history of liver transplant on Mammalian Target Of Rapamycin (mTOR) inhibitor, who attended Emergency department with angio-oedema only on the left side of her tongue. (biomedsearch.com)