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1

Roshanov, Pavel S., Bram Rochwerg, Ameen Patel, et al. "Withholding versus Continuing Angiotensin-converting Enzyme Inhibitors or Angiotensin II Receptor Blockers before Noncardiac Surgery." Anesthesiology 126, no. 1 (2017): 16–27. http://dx.doi.org/10.1097/aln.0000000000001404.

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Abstract Background The effect on cardiovascular outcomes of withholding angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers in chronic users before noncardiac surgery is unknown. Methods In this international prospective cohort study, the authors analyzed data from 14,687 patients (including 4,802 angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker users) at least 45 yr old who had in-patient noncardiac surgery from 2007 to 2011. Using multivariable regression models, the authors studied the relationship between withholding angiotensin-converting e
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2

Farag, Ehab, Chen Liang, Edward J. Mascha, et al. "Association between Use of Angiotensin-converting Enzyme Inhibitors or Angiotensin Receptor Blockers and Postoperative Delirium." Anesthesiology 133, no. 1 (2020): 119–32. http://dx.doi.org/10.1097/aln.0000000000003329.

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Background Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers improve cognitive function. The authors therefore tested the primary hypothesis that preoperative use of angiotensin inhibitors is associated with less delirium in critical care patients. Post hoc, the association between postoperative use of angiotensin system inhibitors and delirium was assessed. Methods The authors conducted a single-site cohort study of adults admitted to Cleveland Clinic critical care units after noncardiac procedures between 2013 and 2018 who had at least one Confusion Assessment Method
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3

Brar, Sandeep, Kathleen D. Liu, Alan S. Go, et al. "Prospective Cohort Study of Renin-Angiotensin System Blocker Usage after Hospitalized Acute Kidney Injury." Clinical Journal of the American Society of Nephrology 16, no. 1 (2020): 26–36. http://dx.doi.org/10.2215/cjn.10840720.

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Background and objectivesThe risk-benefit ratio of angiotensin-converting enzyme inhibitor or angiotensin receptor blocker therapy after AKI may be altered due to concerns regarding recurrent AKI. We evaluated, in a prospective cohort, the association between use (versus nonuse) of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers and the subsequent risk of AKI and other adverse outcomes after hospitalizations with and without AKI.Design, setting, participants, & measurementsWe studied 1538 patients recently discharged from the hospital who enrolled in the multicenter,
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4

Čertíková Chábová, Věra. "Angiotensin converting enzyme inhibitors in nephrology." Klinická farmakologie a farmacie 33, no. 4 (2020): 35–38. http://dx.doi.org/10.36290/far.2019.030.

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5

Li, Ruyin, Tongtong Tang, Feifei Ma, et al. "Identification of Three Novel Angiotensin-I-Converting Enzyme Inhibitory Peptides from Cassia Obtusifolia Seeds and Evaluation of their Inhibition Mechanisms." Current Topics in Nutraceutical Research 22, no. 1 (2023): 108–15. http://dx.doi.org/10.37290/ctnr2641-452x.22:108-115.

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Angiotensin-I-converting enzyme inhibitory peptides were isolated from Cassia obtusifolia seeds by alcalase hydrolysis. Using ultrafiltration, the peptides were divided into four fractions (<1, 1–3, 3–5, >5 kDa). The fraction below 1 kDa exhibited the appropriate ACE inhibition (IC50 = 65.88 μg/mL), and was further purified by gel filtration chromatography, which displayed better angiotensin-I-converting enzyme inhibitory activity (IC50 = 53.67 μg/mL). The amino acid sequences of three novel angiotensin-I-converting enzyme inhibitory peptides were identified by liquid chromatography with
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6

Lazar, Angela Madalina. "Renin-angiotensin-aldosterone system inhibitors – a realm of confusion in COVID-19." Journal of Ideas in Health 4, Special2 (2021): 389–94. http://dx.doi.org/10.47108/jidhealth.vol4.issspecial2.125.

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Currently, there is a persisting dispute regarding the renin-angiotensin-aldosterone-system (RAAS) inhibitors' safety of use in COVID-19 pandemics. On one side, RAAS inhibitors appear to determine an overexpression of ACE2, the receptor of SARS-CoV-2. Therefore, they could increase the risk of SARS-CoV-2 infection and its degree of severity. On the other side, the discontinuation of RAAS leads to cardiovascular decompensation and has been discouraged by the major medical societies. Also, large-cohort studies report beneficial or at least neutral effects for the RAAS inhibitors in COVID-19 pati
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7

Warner, Kelly K., James A. Visconti, and Marva M. Tschampel. "Angiotensin II Receptor Blockers in Patients with ACE Inhibitor–Induced Angioedema." Annals of Pharmacotherapy 34, no. 4 (2000): 526–28. http://dx.doi.org/10.1345/aph.19294.

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OBJECTIVE: To determine the safety of using angiotensin II receptor blockers in patients who have experienced angioedema following treatment with angiotensin-converting enzyme (ACE) inhibitors. DATA SOURCES: Clinical literature identified through MEDLINE (January 1966–August 1999). Key search terms included angioneurotic edema, angiotensin-converting enzyme inhibitors, receptors–angiotensin, and losartan. DATA SYNTHESIS: ACE inhibitor–induced angioedema occurs with an incidence of 0.1–0.5%. Alternative therapy is necessary for patients who experience this potentially life-threatening adverse e
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8

Mets, Berend, and Edward D. Miller. "Angiotensin and angiotensin-converting enzyme inhibitors." Baillière's Clinical Anaesthesiology 8, no. 1 (1994): 151–73. http://dx.doi.org/10.1016/s0950-3501(05)80142-4.

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9

Leclézio, Alexandra, Jared Robinson, and Indrajit Banerjee. "SARS-CoV-2: ACE inhibitors, disastrous or desirable?" Journal of Biomedical Sciences 7, no. 1 (2020): 40–46. http://dx.doi.org/10.3126/jbs.v7i1.29852.

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Background: The world has a current total of 6,663,304 confirmed cases of COVID-19 with a death count of 392,802 deaths according to the WHO (6 June 2020). Various risk factors for the acquisition and subsequent development of deadly complications due to the virus have been established. One such risk factor is the presence of cardiovascular disease, particularly hypertension as a comorbidity. It must be noted that JNC 8 advise the use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers as first line drugs for the management of hypertension. ARDS is caused by the activa
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10

Shunan, Fan, Yuan Jiqing, and Dong Xue. "Effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers on cardiovascular events in patients with diabetes and overt nephropathy: a meta-analysis of randomised controlled trials." Journal of the Renin-Angiotensin-Aldosterone System 19, no. 4 (2018): 147032031880349. http://dx.doi.org/10.1177/1470320318803495.

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Objective: The efficacy of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in reducing cardiovascular outcomes in patients with diabetes and overt nephropathy is still a controversial issue. Methods: We systematically searched MEDLINE, Embase and Cochrane Library for randomised controlled trials. Results: Thirteen trials containing 4638 patients with diabetes and overt nephropathy were included. Compared with controls, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker treatment did not reduce the risk of cardiovascular events (odds ratio 0.94, 95%
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11

Yang, Hong, Xiangyu Wang, and Mohan K. Raizada. "Characterization of Signal Transduction Pathway in Neurotropic Action of Angiotensin II in Brain Neurons." Endocrinology 142, no. 8 (2001): 3502–11. http://dx.doi.org/10.1210/endo.142.8.8348.

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Abstract Interaction of angiotensin II with the neuronal angiotensin type 1 receptor stimulates the PI3K signaling pathway. Our objective in this study was to investigate the hypothesis that the PI3K cascade regulates the neurotropic actions of angiotensin II in rat brain neurons. We followed growth associated protein-43 expression and neurite extension as markers of neurotropic activity. Angiotensin II, through its interaction with the angiotensin type 1 receptor, increased growth associated protein-43 expression and neurite extension. These effects were abolished by pretreatment of neurons w
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12

Kukes, V. G., and G. S. Anikin. "The effectiveness of zofenopril in patients with cardiovascular disease." Systemic Hypertension 11, no. 2 (2014): 59–62. http://dx.doi.org/10.26442/sg29028.

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Hyperactivity of the renin-angiotensin-aldosterone system plays an important role in the pathogenesis of any cardiovascular disease. Angiotensin - converting enzyme inhibitors are the main drugs among many medicines influencing the activity of the renin-angiotensin-aldosterone system, and these inhibitors have a wide range of beneficial effects. The presence of the sulfhydryl group in a molecule of angiotensin-converting enzyme inhibitor (zofenopril) determines the number of unique properties of this drug. Recent results have been showing the effectiveness of treatment in case of combined card
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13

Bastać, Dušan, Zoran Joksimović, Snežana Pavlović, Mila Bastać, Anastasija Raščanin, and Igor Đorđioski. "Paradigm change in the treatment of chronic heart failure according to ESC Guide 2021: New innovative drugs in focus." Timocki medicinski glasnik 47, no. 1 (2022): 40–47. http://dx.doi.org/10.5937/tmg2201040b.

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Medical, primarily drug therapy directed by the New ESC Guide or Guidelines for Patients with Heart Failure (HF) brings significant innovations and changes in the treatment paradigm, from the gradual introduction of drugs to the simultaneous introduction of 5 main classes of drugs. Treatment of heart failure with reduced left ventricular ejection fraction (HFrEF) and symptoms of class II-New York Heart Association (NYHA) -dispnea at higher exertion and higher NYHA classes, now includes angiotensin receptor inhibitor neprilysin (ARNI) as a substitute for angiotenzin convertase enzyme inhibitor(
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14

KATUGAMPOLA, Sidath D., and Anthony P. DAVENPORT. "Radioligand binding reveals chymase as the predominant enzyme for mediating tissue conversion of angiotensin I in the normal human heart." Clinical Science 102, no. 1 (2001): 15–21. http://dx.doi.org/10.1042/cs1020015.

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We investigated the binding characteristics of angiotensin receptors and used this assay to determine the predominant enzyme capable of converting angiotensin I in the human left ventricle. In homogenates of human left ventricle, 125I-[Sar1,Ile8]angiotensin II bound with sub-nanomolar affinity, with a corresponding KD of 0.42±0.09nM, a Bmax of 11.2±2.3fmolċmg-1 protein and a Hill slope of 1.04±0.04. The rank order of inhibitory potency of competing ligands for the 125I-[Sar1,Ile8]angiotensin II binding site was CGP42112 > angiotensin II⩾ angiotensin III = angiotensin I > losartan. The an
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15

Schalekamp, Maarten A. D. H., Frans H. M. Derkx, and Anton H. van den Meiracker. "Renin inhibitors, angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists." Journal of Hypertension 10, Sup 7 (1992): S157???164. http://dx.doi.org/10.1097/00004872-199212000-00017.

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16

Maarten, A. D. H., and Frans Schalekamp. "Renin inhibitors, angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists." Journal of Hypertension 10 (1992): S165. http://dx.doi.org/10.1097/00004872-199212007-00017.

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17

Cobb, Christopher S., John Rundle, Susan C. Frankling, and J. Anne Brown. "Angiotensin I-converting enzyme-like activity in a cephalochordate." Journal of the Marine Biological Association of the United Kingdom 83, no. 6 (2003): 1307–8. http://dx.doi.org/10.1017/s0025315403008725.

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The presence of angiotensin I-converting enzyme-like activity (ACELA) was investigated in whole body homogenates of Branchiostoma lanceolatum using a highly sensitive fluorimetric assay. The measured enzyme activity was inhibited by the two angiotensin converting enzyme inhibitors, captopril and enalapril, suggesting a biochemical pathway that could generate the angiotensins observed in the central nervous system of amphioxus.
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18

De Lombaert, Stephane, Ricardo E. Chatelain, Cynthia A. Fink, and Angelo J. Trapani. "Design and Pharmacology of Dual Angiotensin-Converting Enzyme and Neutral Endopeptidase Inhibitors." Current Pharmaceutical Design 2, no. 5 (1996): 443–62. http://dx.doi.org/10.2174/1381612802666221004171525.

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Angiotensin converting enzyme (ACE) inhibitors are important therapeutic agents for the management of hypertension and congestive heart failure (CHF). Although the therapeutic effects of neutral endopeptidase (NEP) inhibitors (i.e. blood pressure lowering, natriuresis, diuresis) in patients have been unimpressive, experimental and clinical evidence suggests that concomitant blockade of the renin-angiotensin­ aldosterone system (RAAS) would be beneficial. Therefore, with the expectation that combined inhibition of ACE and NEP could provide therapeutic advantages over selective inhibitors of eit
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19

Pryde, P. G., A. B. Sedman, C. E. Nugent, and M. Barr. "Angiotensin-converting enzyme inhibitor fetopathy." Journal of the American Society of Nephrology 3, no. 9 (1993): 1575–82. http://dx.doi.org/10.1681/asn.v391575.

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Angiotensin-converting enzyme (ACE) inhibitors are widely used for controlling hypertension. Their use in women who are pregnant is not without risk to the fetus. We describe three infants exposed in utero to ACE inhibitors who had adverse outcomes. These cases, combined with other reports in the literature, suggest strongly that these drugs are fetotoxic. ACE inhibitor fetopathy is characterized by fetal hypotension, anuria-oligohydramnios, growth restriction, pulmonary hypoplasia, renal tubular dysplasia, and hypocalvaria. Although the true frequency of adverse fetal effects has yet to be de
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20

Finnegan, Patrick M., and Brenda L. Gleason. "Combination ACE Inhibitors and Angiotensin II Receptor Blockers for Hypertension." Annals of Pharmacotherapy 37, no. 6 (2003): 886–89. http://dx.doi.org/10.1345/aph.1c393.

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OBJECTIVE: To review data concerning combined angiotensin-converting enzyme (ACE) inhibitor and angiotensin II receptor blocker (ARB) therapy for hypertension. DATA SOURCES: MEDLINE (1966–April 2003), IPA (1970–April 2003), and EMBASE (1974–April 2003) with search terms of ACE inhibitor, angiotensin receptor blocker, essential hypertension, and combination therapy. DATA SYNTHESIS: ACE inhibitors provide incomplete blockade of the renin–angiotensin system, sometimes leading to loss of blood pressure control. Addition of ARBs may in theory further reduce blood pressure. Studies of combined ACE i
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21

Verdecchia, Paolo, Fabio Angeli, and Gianpaolo Reboldi. "Good News from Aliskiren?" Clinical Medicine. Therapeutics 1 (January 2009): CMT.S2862. http://dx.doi.org/10.4137/cmt.s2862.

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The renin-angiotensin system can be inhibited through inhibition of angiotensin I generation from angiotensinogen by direct renin inhibitors, inhibition of angiotensin II generation from angiotensin I by angiotensin-converting enzyme inhibitors and by direct inhibition of the action of angiotensin II receptor level. Aliskiren, the first direct renin inhibitor to reach the market, is a low molecular weight, orally active, hydrophilic nonpeptide. It blocks angiotensin I generation, while plasma renin concentration increases because the drugs blocks the negative feed-back exerted by angiotensin I
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22

Jutte, Sara B., and Jon E. Sprague. "Pharmacologic Regulation of the Renin—Angiotensin System: Physiologic and Pathologic Effects." Journal of Pharmacy Technology 16, no. 4 (2000): 138–46. http://dx.doi.org/10.1177/875512250001600408.

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Objective: To review the physiologic and pathologic roles of the renin-angiotensin system in maintaining blood pressure, glomerular filtration rate, and myocardial tissue growth. The pharmacologic regulations of the pathologic effects of the renin-angiotensin system are emphasized, with a comparison between angiotensin-converting enzyme (ACE) inhibitors and angiotensin1 receptor (AT1) antagonists. Data Sources: English-language basic science, clinical studies, and review articles were identified using MEDLINE, IOWA, and a manual search from January 1966 through September 1999. References were
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23

Ptasinska-Wnuk, Dorota, Hanna Lawnicka, Slawomir Mucha, Jolanta Kunert-Radek, Marek Pawlikowski, and Henryk Stepien. "Angiotensins Inhibit Cell Growth in GH3 Lactosomatotroph Pituitary Tumor Cell Culture: A Possible Involvement of the p44/42 and p38 MAPK Pathways." Scientific World Journal 2012 (2012): 1–10. http://dx.doi.org/10.1100/2012/189290.

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The local renin-angiotensin system is present in the pituitary. We investigated the effects of angiotensins on GH3 lactosomatotroph cells proliferation in vitro and the involvement of p44/42 and p38 MAPK inhibitors in the growth-regulatory effects of angiotensins.Materials and Methods. Cell viability using the Mosmann method and proliferation by the measurement of BrdU incorporation during DNA synthesis were estimated.Results. Ang II and ang IV decreased the viability and proliferation of GH3 cells. Inhibitor of p44/42 MAPK attenuated the effects of ang II on cell viability and proliferation b
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24

Ripley, Toni L. "Valsartan in Chronic Heart Failure." Annals of Pharmacotherapy 39, no. 3 (2005): 460–69. http://dx.doi.org/10.1345/aph.1e327.

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OBJECTIVE: To evaluate the evidence for valsartan in the treatment of heart failure and determine its need for formulary inclusion. DATA SOURCES: OVID and PubMed databases were searched (1983–June 2004) using the key words angiotensin-receptor blocker, heart failure, valsartan, Diovan, and angiotensin-converting enzyme inhibitor. Only English-language literature was selected. STUDY SELECTION AND DATA EXTRACTION: Pharmacology and pharmacokinetic evaluations for valsartan were selected. Prospective, randomized clinical trials investigating the use of valsartan and other angiotensin-receptor bloc
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25

Imanishi, Toshio, Hiroto Tsujioka, and Takashi Akasaka. "Hypertension Management and End Organ Protection: Focus on Aliskiren." Clinical Medicine. Therapeutics 1 (January 2009): CMT.S1980. http://dx.doi.org/10.4137/cmt.s1980.

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The renin-angiotensin system (RAS) activity is a key factor in the pathophysiology and development of hypertension, atherosclerosis, heart failure, and renal disease. It is unclear whether angiotensin-converting-enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs) have fully delivered the expected reductions in cardiovascular risk. In fact, the optimized RAS suppression is difficult to achieve with these agents, partly because ACE inhibitors and ARBs both activate compensatory feedback mechanisms that result in renin release and increase plasma renin activity (PRA). Molecular model
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26

Dettlaff-Pokora, Agnieszka, and Julian Swierczynski. "Dysregulation of the Renin-Angiotensin-Aldosterone System (RAA) in Patients Infected with SARS-CoV-2-Possible Clinical Consequences." International Journal of Molecular Sciences 22, no. 9 (2021): 4503. http://dx.doi.org/10.3390/ijms22094503.

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SARS-CoV-2 impairs the renin-angiotensin-aledosterone system via binding ACE2 enzyme. ACE2 plays a key role in the biosynthesis of angiotensin (1-7), catalyzing the conversion of angiotensin 2 into angiotensin (1-7) and the reaction of angiotensin synthesis (1-9), from which angiotensin is (1-7) produced under the influence of ACE (Angiotensin-Converting Enzyme). Angiotensin 2 is a potent vasoconstrictor and atherogenic molecule converted by ACE2 to reducing inflammation and vasodilating in action angiotensin (1-7). Angiotensin (1-9), that is a product of angiotensin 1 metabolism and precursor
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27

Belz, Gustav G., Wilhelm Kirch, and Cornelis H. Kleinbloesem. "Angiotensin-Converting Enzyme Inhibitors." Clinical Pharmacokinetics 15, no. 5 (1988): 295–318. http://dx.doi.org/10.2165/00003088-198815050-00003.

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28

Herlihy, BL, and JT Herlihy. "Angiotensin-converting enzyme inhibitors." Critical Care Nurse 10, no. 3 (1990): 74–77. http://dx.doi.org/10.4037/ccn1990.10.3.74.

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29

Peng, Hongmei, Oscar A. Carretero, Nikola Vuljaj, et al. "Angiotensin-Converting Enzyme Inhibitors." Circulation 112, no. 16 (2005): 2436–45. http://dx.doi.org/10.1161/circulationaha.104.528695.

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30

Kuhn, Merrily. "Angiotensin-Converting Enzyme Inhibitors." AACN Advanced Critical Care 3, no. 2 (1992): 461–71. http://dx.doi.org/10.4037/15597768-1992-2017.

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The angiotensin-converting enzyme (ACE) inhibitors available today include Captopril (Capoten), enalapril (Vasotec), enaloprilat (Vasotec IV), lisinopril (Prinivil, Zestril), benazepril (Lotensin), fosinopril (Monopril), and ramipril (Atace). These drugs are used in the treatment of hypertension and congestive heart failure. They also are used in treating renovascular hypertension not amenable to surgery and are being studied to decrease left ventricular size after infarction and to determine whether they slow the rate of internal hyperplasia. Angiotensin-converting enzyme inhibitors have nega
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31

Jackson, Bruce, Rose Cubela, and Colin I. Johnston. "Angiotensin-Converting Enzyme Inhibitors." Journal of Cardiovascular Pharmacology 9, no. 6 (1987): 699–704. http://dx.doi.org/10.1097/00005344-198706000-00010.

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32

Nelson, Edward B. "Angiotensin-Converting Enzyme Inhibitors." Critical Care Medicine 17, no. 3 (1989): 302. http://dx.doi.org/10.1097/00003246-198903000-00029.

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33

Cody, Robert J. "Angiotensin-Converting Enzyme Inhibitors." Cardiology in Review 2, no. 3 (1994): 145–56. http://dx.doi.org/10.1097/00045415-199405000-00005.

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34

Gavras, Haralambos, and Irene Gavras. "Angiotensin converting enzyme inhibitors." Journal of Hypertension 9, no. 11 (1991): 1075. http://dx.doi.org/10.1097/00004872-199111000-00015.

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35

Izzo Jr, Joseph L., and Matthew R. Weir. "Angiotensin-Converting Enzyme Inhibitors." Journal of Clinical Hypertension 13, no. 9 (2011): 667–75. http://dx.doi.org/10.1111/j.1751-7176.2011.00508.x.

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36

Lombardi, William L., and Sheldon E. Litwin. "Angiotensin-converting enzyme inhibitors." Coronary Artery Disease 10, no. 6 (1999): 361–68. http://dx.doi.org/10.1097/00019501-199909000-00003.

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37

Brown, Nancy J., and Douglas E. Vaughan. "Angiotensin-Converting Enzyme Inhibitors." Circulation 97, no. 14 (1998): 1411–20. http://dx.doi.org/10.1161/01.cir.97.14.1411.

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38

Macdonald, Graham. "Angiotensin‐Converting enzyme inhibitors." Medical Journal of Australia 160, no. 5 (1994): 279–81. http://dx.doi.org/10.5694/j.1326-5377.1994.tb125832.x.

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39

Kostis, John B. "Angiotensin-Converting Enzyme Inhibitors." American Journal of Hypertension 2, no. 1 (1989): 57–64. http://dx.doi.org/10.1093/ajh/2.1.57.

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40

Bauer, J. H. "Angiotensin Converting Enzyme Inhibitors." American Journal of Hypertension 3, no. 4 (1990): 331–37. http://dx.doi.org/10.1093/ajh/3.4.331.

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41

Rotmensch, Heschi H., Peter H. Vlasses, and Roger K. Ferguson. "Angiotensin-Converting Enzyme Inhibitors." Medical Clinics of North America 72, no. 2 (1988): 399–425. http://dx.doi.org/10.1016/s0025-7125(16)30776-3.

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42

Weinberger, Myron H. "Angiotensin-Converting Enzyme Inhibitors." Medical Clinics of North America 71, no. 5 (1987): 979–90. http://dx.doi.org/10.1016/s0025-7125(16)30821-5.

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43

Fitz, Annette. "ANGIOTENSIN CONVERTING ENZYME INHIBITORS." Chest 94, no. 4 (1988): 27. http://dx.doi.org/10.1016/s0012-3692(16)30553-0.

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44

Abraham, Anil, and Eugene Farber. "Angiotensin-converting enzyme inhibitors." Journal of the American Academy of Dermatology 29, no. 6 (1993): 1061. http://dx.doi.org/10.1016/s0190-9622(08)82060-9.

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45

Litt, Jerome Z. "Angiotensin-converting enzyme inhibitors." Journal of the American Academy of Dermatology 29, no. 6 (1993): 1062. http://dx.doi.org/10.1016/s0190-9622(08)82061-0.

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46

Rabito, Sara F. "Angiotensin-converting enzyme inhibitors." Journal of the American Academy of Dermatology 30, no. 4 (1994): 671–72. http://dx.doi.org/10.1016/s0190-9622(09)80127-8.

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47

Nyman, C. R. "Angiotensin converting enzyme inhibitors." British Journal of Diseases of the Chest 82 (January 1988): 324. http://dx.doi.org/10.1016/0007-0971(88)90078-2.

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48

Scott, Robert A., and David B. Barnett. "Angiotensin converting enzyme Inhibitors." American Heart Journal 118, no. 6 (1989): 1358. http://dx.doi.org/10.1016/0002-8703(89)90050-1.

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49

Yachnyk, I. M., N. P. Karpenko, O. V. Kushneryk, and N. M. Tarasenko. "Angiotensin-converting enzyme inhibitors." Medicine of Ukraine, no. 9-10(265-6) (December 20, 2022): 44–48. http://dx.doi.org/10.37987/1997-9894.2022.9-10(265-6).271850.

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The article reflects the issues of pharmacology and pharmacokinetics of the use of drugs belonging to the group of angiotensin – converting enzyme inhibitors. Given the high risks to the life of children and adults, the clinician must have knowledge of the classification, mechanism of action and possible side effects of this group of drugs.
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50

Melchior, Wayne R., Vinita Bindlish, and Linda A. Jaber. "Angiotensin-Converting Enzyme Inhibitors in Diabetic Nephropathy." Annals of Pharmacotherapy 27, no. 3 (1993): 344–50. http://dx.doi.org/10.1177/106002809302700318.

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OBJECTIVE: Diabetic nephropathy (DN) is a leading cause of kidney disease in the US. At least four factors influence whether people with diabetes will develop DN: (1) hypertension, (2) hyperglycemia, (3) dietary protein intake, and (4) intrarenal hemodynamics. The angiotensin-converting enzyme (ACE) inhibitors are known to affect blood pressure (BP) and intrarenal hemodynamics; thus, they may prevent the onset of DN or slow the decline in renal function once DN has been diagnosed. DATA SOURCES: English-language, controlled, and crossover studies published between 1973 and 1991 and indexed in M
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