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Journal articles on the topic 'Captoprill'

Author: Grafiati

Published: 5 June 2025

Last updated: 2 August 2025

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1

Zucker, I. H., J. S. Chen, and W. Wang. "Renal sympathetic nerve and hemodynamic responses to captopril in conscious dogs: role of prostaglandins." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 1 (1991): H260—H266. http://dx.doi.org/10.1152/ajpheart.1991.260.1.h260.

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The angiotensin converting enzyme inhibitor captopril has been shown to cause resetting of the arterial baroreflex to a lower pressure without a change in gain. The present study was conducted to determine whether captopril altered the relationship between arterial pressure, heart rate, and renal sympathetic nerve activity in conscious quietly resting dogs. Fourteen instrumented dogs were given 2 mg/kg iv of captopril; 10 min later postcaptopril measurements were made. Six of the fourteen dogs were pretreated with cyclooxygenase inhibitor (indomethacin or meclofenamate) before administration o

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2

Horseman, Timothy, W. Bradley Rittase, John E. Slaven, et al. "Ferroptosis, Inflammation, and Microbiome Alterations in the Intestine in the Göttingen Minipig Model of Hematopoietic-Acute Radiation Syndrome." International Journal of Molecular Sciences 25, no. 8 (2024): 4535. http://dx.doi.org/10.3390/ijms25084535.

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Hematopoietic acute radiation syndrome (H-ARS) involves injury to multiple organ systems following total body irradiation (TBI). Our laboratory demonstrated that captopril, an angiotensin-converting enzyme inhibitor, mitigates H-ARS in Göttingen minipigs, with improved survival and hematopoietic recovery, as well as the suppression of acute inflammation. However, the effects of captopril on the gastrointestinal (GI) system after TBI are not well known. We used a Göttingen minipig H-ARS model to investigate captopril’s effects on the GI following TBI (60Co 1.79 or 1.80 Gy, 0.42–0.48 Gy/min), wi

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3

Sastrosubroto, Hardiman, Santosa Soeroso, and Eriyati Indrasanto. "Captopril Treatment in Rheumatic Heart Disease with Congestive Heart Failure A Preliminary Report." Paediatrica Indonesiana 29, no. 9-10 (2018): 209–14. http://dx.doi.org/10.14238/pi29.9-10.1989.209-14.

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A small scale controlled trial of captopril (ACE inhibitor) was conducted in 8 children with congestive heart failure due to rheumatic mitral regurgitation with or without mild mitral stenosis. The age of the patient ranged from 5.5 to 13 years (mean 9,3 years). Four children, served as control group, received digitalis and diuretics as standard treatment; while the other 4 children also received 2 x 12,5 mg of captopril in addition to standard treatment. The effect of both regimens were measured by usingchanges of left ventricular function as seen on the echocardiogram performed before treatm

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4

Rademaker, Miriam T., Christopher J. Charles, M. Gary Nicholls, and A. Mark Richards. "Urocortin 2 combined with angiotensin-converting enzyme inhibition in experimental heart failure." Clinical Science 114, no. 10 (2008): 635–42. http://dx.doi.org/10.1042/cs20070364.

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Ucn2 (urocortin 2) is a recently discovered peptide with therapeutic potential in heart failure. As any new treatment is likely to be used in conjunction with standard ACEI (angiotensin-converting enzyme inhibitor) therapy, it is important that the combined effects of these agents are assessed. In the present study, we investigated the effects of Ucn2 and an ACEI (captopril) administered for 3 h, both separately and together, in eight sheep with pacing-induced heart failure. Ucn2 and captopril alone both increased CO (cardiac output; Ucn2>captopril) and decreased arterial pressure (captopri

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5

Allon, M., C. B. Pasque, and M. Rodriguez. "Interaction of captopril and ibuprofen on glomerular and tubular function in humans." American Journal of Physiology-Renal Physiology 259, no. 2 (1990): F233—F238. http://dx.doi.org/10.1152/ajprenal.1990.259.2.f233.

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Renal hemodynamics and tubular solute and water handling were evaluated in normal subjects during water diuresis, before and after the acute administration of captopril, ibuprofen, or the combination of both drugs. The glomerular filtration increased after captopril administration but did not change after ibuprofen alone or in combination with captopril. Renal plasma flow increased with captopril alone and captopril plus ibuprofen but did not change after ibuprofen alone. Urine volume and Na excretion increased with captopril and decreased after ibuprofen; coadministration of ibuprofen attenua

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Campbell, B. C., Alessandra Sturani, and J. L. Reid. "Evidence of Parasympathetic Activity of the Angiotensin Converting Enzyme Inhibitor, Captopril, in Normotensive Man." Clinical Science 68, no. 1 (1985): 49–56. http://dx.doi.org/10.1042/cs0680049.

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1. Captopril (50 mg orally) produced a significant fall in systolic and diastolic blood pressure in six normotensive sodium replete subjects, without a rise in heart rate. 2. On captopril, there was no change in the expected normal increase in heart rate on standing. Supine plasma noradrenaline was not reduced by captopril and normal postural increases were maintained. 3. Atropine (0.04 mg/kg i.v.) reduced the difference in blood pressure change between captopril and placebo. 4. Facial immersion in water produced a bradycardia. This change was abolished by atropine and attenuated both by capto

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Tatiane, de Medeiros, de S. Dantas Deyse, and F. de Farias Robson. "Cu (II) and Hg(II) captopril compounds in aqueous media: A calorimetric study." Chemistry Research Journal 1, no. 4 (2016): 154–56. https://doi.org/10.5281/zenodo.13995612.

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The interactions in aqueous solution of captopril with Cu(II) and Hg(II) cations are investigated through solution calorimetry. The reactions and respective enthalpy values (kJ mol<sup>-1</sup>) are: Cu<sup>2+</sup> (aq) + Captopril (aq) → [Cu.Captopril]<sup>2+</sup> (aq), -27,25; Cu<sup>2+</sup> (aq) + 2 Captopril (aq) → [Cu.2 Captopril]<sup>2+</sup> (aq), -28,37 and Hg<sup>2+</sup> (aq) + Captopril (aq) → [Hg.Captopril (aq)]<sup>2+</sup> (aq), -90,34. The soft acid-soft base: Hg(II)-S interaction it is pointed out as the main responsible for the higher captopril-Hg(II) interac

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8

Shindo, K., J. R. Baker, D. A. Munafo, and T. D. Bigby. "Captopril inhibits neutrophil synthesis of leukotriene B4 in vitro and in vivo." Journal of Immunology 153, no. 12 (1994): 5750–59. http://dx.doi.org/10.4049/jimmunol.153.12.5750.

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Abstract The aim of this investigation was to determine the effects of metalloproteinase inhibitors on leukotriene (LT) A4 hydrolase in human neutrophil cytosol and to examine the effects of captopril on intact neutrophils in vitro and in vivo. Cytosolic fractions were assayed for LTA4 hydrolase and 5-lipoxygenase activity in the presence or absence of inhibitors. Only bestatin, 1,10-O-phenanthroline, captopril and fosinoprilat demonstrated significant effects. The IC50 of captopril and fosinoprilat for LTA4 hydrolase activity were 500 microM and 1 mM, respectively. No inhibition of 5-lipoxyge

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Lewis, R. M., M. H. Vickers, D. C. Batchelor, N. S. Bassett, B. M. Johnston, and S. J. M. Skinner. "Effects of maternal captopril treatment on growth, blood glucose and plasma insulin in the fetal spontaneously hypertensive rat." Reproduction, Fertility and Development 11, no. 8 (1999): 403. http://dx.doi.org/10.1071/rd99081.

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In the spontaneously hypertensive rat (SHR) fetal growth and metabolism are abnormal. It has been speculated that maternal hypertension may be the cause of these abnormalities. Captopril treatment, which reduces maternal blood pressure, during pregnancy and lactation, is reported to have a beneficial effect postnatally, normalizing the blood pressure of offspring in the SHR. In the present study, the effects of maternal captopril treatment on fetal growth and plasma metabolites were investigated in the fetuses of two rat strains (SHR and Wistar-Kyoto (WKY)), in order to determine whether norma

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Kurniawan, Wikan, Marsetyawan Heparis Nur Ekandaru Soesatyo та Teguh Aryandono. "The effects of docetaxel and/or captopril in expression of TGF-β1, MMP-1, CTGF, and PAI-1 as markers of anterior urethral stricture in an animal model". Therapeutic Advances in Urology 12 (січень 2020): 175628722092799. http://dx.doi.org/10.1177/1756287220927994.

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Background: Treatment of urethral trauma is currently done after urethral stricture occurs. Stricture therapy after occurrence gives unsatisfactory success rates. Several genes, such as transforming growth factor beta 1 (TGF-β1), matrix metalloproteinase 1 (MMP-1), connective tissue growth factor (CTGF), and plasminogen activator inhibitor 1 (PAI-1), have a proven role in urethral stricture development. The purpose of this study was to assess the effect docetaxel and/or captopril on the RNA expression of those genes. Methods: The subjects of this research were 26 male New Zealand rabbits aged

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11

Mallet, Louise, James W. Cooper, and Joyce Thomas. "Bullous Pemphigoid Associated with Captopril." DICP 23, no. 1 (1989): 63. http://dx.doi.org/10.1177/106002808902300115.

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Captopril is commonly prescribed to patients with hypertension and congestive heart failure. Adverse dermatological reactions have been reported in about ten percent of patients receiving captopril. This case report describes a 77-year-old white woman who developed bullous pemphigoid associated with the use of captopril. The patient presented with bullous eruptions localized on the palms of both hands about 50 days after captopril 25 mg bid was started. Biopsy report was consistent with bullous pemphigoid. Captopril therapy was discontinued and the lesions healed after oral corticosteroid ther

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Darma, Nanda Aflyona, Roslinda Rasyid, and Harrizul Rivai. "Overview of the Determination of Captopril Levels in Pharmaceutical Preparations and Biological Matrices." International Journal of Pharmaceutical Sciences and Medicine 6, no. 4 (2021): 1–11. http://dx.doi.org/10.47760/ijpsm.2021.v06i04.001.

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Captopril is the most commonly prescribed ACE-Inhibitor class of drugs because it is easily accessible and affordable. Therefore, to ensure drug quality, captopril levels were determined. This review article aims to provide an overview of the various analytical techniques that have been carried out in selecting the groups of captopril in both pharmaceutical dosage forms and biological matrices. Some of these analytical methods include the UV-Visible spectrophotometric method, high-performance liquid chromatography (HPLC), voltammetry, and flow injection. The data collection process in this rev

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Silwal, Surendra. "Ineffectiveness of D-captopril as an Inhibitor Against VIM-31 Metallo-β-lactamase Due to a Single Mutation Near Its Active Site". Structural Dynamics 12, № 2_Supplement (2025): A78. https://doi.org/10.1063/4.0000387.

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Activity assays and X-ray crystallographic studies were undertaken to elucidate the inhibitory mechanism of captopril stereoisomers on Verona integron-encoded metallo-β-lactamases, specifically VIM-20, VIM-31, and VIM-15. All three VIM-2-like variants (VIM-20, VIM-31, and VIM-15) and VIM-2 expressed in Escherichia coli exhibited catalytic activity with comparable steady-state kinetic parameters. Among the tested thiol drugs (L- and D-captopril, DL-thiorphan, and 2,3-dimercaprol), IC50 analyses indicated that D-captopril and 2,3-dimercaprol were more potent inhibitors against the VIM enzymes ex

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RADEMAKER, Miriam T., Chris J. CHARLES, Garth J. S. COOPER, et al. "Combined angiotensin-converting enzyme inhibition and adrenomedullin in an ovine model of heart failure." Clinical Science 102, no. 6 (2002): 653–60. http://dx.doi.org/10.1042/cs1020653.

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Advances in the treatment of heart failure may require manipulation of neurohumoral responses to cardiac impairment in addition to the established strategy of angiotensin-converting enzyme (ACE) inhibition. Importantly, since new treatments are likely to be used in conjunction with ACE inhibition therapy, the effects of the combination of agents need to be assessed. Adrenomedullin (ADM) is a peptide with potent vasodilator and natriuretic actions. ADM and an ACE inhibitor (captopril) were administered for 3h both separately and together in eight sheep with heart failure. Both ADM and captopril

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15

Smith, S. R., T. M. Coffman, and L. P. Svetkey. "Effect of low-dose aspirin on thromboxane production and the antihypertensive effect of captopril." Journal of the American Society of Nephrology 4, no. 5 (1993): 1133–39. http://dx.doi.org/10.1681/asn.v451133.

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Some of the antihypertensive effects of angiotensin-converting enzyme (ACE) inhibitors occur through nonangiotensin II-mediated mechanisms. One of these is through decreased kinin degradation, leading to enhanced production of vasodilator arachidonic acid metabolites. It was reasoned that if ACE inhibition also leads to an increase in the production of the potent vasoconstrictor thromboxane A2, then maneuvers that selectively inhibit thromboxane production without reducing prostaglandins (PG) E2 + PGI2 might enhance the antihypertensive effect of ACE inhibition. This double-blinded, randomized

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Ruksin, V. V., O. V. Grishin, M. M. Chiritso, A. N. Malakhov, and M. V. Onuchin. "EFFICACY OF CAPTOPRIL, MOXONIDINE AND THEIR COMBINATIONS WITH NIFEDIPINE IN THE NON-THREATENING HYPERTENSION." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 19, no. 1 (2013): 59–65. http://dx.doi.org/10.18705/1607-419x-2013-19-1-59-65.

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Objective. To study several medications and their combinations in non-threatened hypertension worsening captopril, and moxonidine, captopril + nifedipine, captopril + moxonidine.Design and methods. We include326 patients (253 females) aged 45–89 years who referred for the urgent health care due to the non-threatene hypertension worsening. Mean duration of hypertension was 20,6 ± 0,6 years. Special questionnaires were ﬁlle in, heart rate, blood pressure by Korotkoff method, and electrocardiogram were registered.Results. Moxonidinwas shown to be more effective in patients with the sympathetic hy

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17

van Baak, MA, FM Koene, FT Verstappen, and ES Tan. "Exercise performance during captopril and atenolol treatment in hypertensive patients." British Journal of Clinical Pharmacology 32, no. 6 (1991): 723–28. http://dx.doi.org/10.1111/j.1365-2125.1991.tb03980.x.

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1. Maximal aerobic exercise capacity, submaximal endurance exercise performance, and exercise haemodynamics have been studied in sixteen patients with mild to moderate essential hypertension during treatment with captopril and atenolol. 2. Administration of atenolol (1 x 100 mg day‐1) or captopril (1 x 100 mg day‐1) for 6 weeks resulted in similar supine and erect systolic and diastolic blood pressures. Heart rate was significantly lower during atenolol treatment. 3. Exercise heart rate and systolic blood pressure were significantly lower during atenolol than during captopril treatment, exerci

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18

Dolatabadi, Maryam, Ruhollah Akbarpour, and Saeid Ahmadzadeh. "Catalytic ozonation process using ZnO/Fe2O3 nanocomposite for efficient removal of captopril from aqueous solution." Analytical Methods in Environmental Chemistry Journal 5, no. 03 (2022): 31–39. http://dx.doi.org/10.24200/amecj.v5.i03.197.

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The presence of pharmaceutical compounds in aqueous media, even in low concentrations, has caused adverse effects on human, animal, and environmental health. Captopril is a widely used pharmaceutical compound detected in the environment at different concentrations. Because of the concern and problems caused by the presence of captopril in water and the aquatic ecosystem, it appears necessary to remove it from the environment. The current study investigated captopril removal by a catalytic ozonation process using ZnO/Fe2O3 nanocomposite as a low-cost catalyst. The effects of variables such as Z

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Wade, C. E., S. R. Ramee, M. M. Hunt, and C. J. White. "Hormonal and renal responses to converting enzyme inhibition during maximal exercise." Journal of Applied Physiology 63, no. 5 (1987): 1796–800. http://dx.doi.org/10.1152/jappl.1987.63.5.1796.

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The role of angiotensin II in the hormonal and renal responses to maximal exercise was investigated by using the angiotensin-converting enzyme inhibitor captopril. Nine male subjects performed a standardized maximal treadmill test with and without acute captopril treatment (25 mg orally). At rest, captopril elevated plasma renin activity and lowered aldosterone levels. With maximal exercise, captopril treatment reduced the increase in mean arterial blood pressure by 8 mmHg and the increase in plasma renin activity by 3.0 ng ANG I.ml-1.h-1. The responses of adrenocorticotropin (ACTH), cortisol,

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Bahramipur, Hossein, and Fahimeh Jalali. "Voltammetric Determination of Captopril Using Chlorpromazine as a Homogeneous Mediator." International Journal of Electrochemistry 2011 (2011): 1–6. http://dx.doi.org/10.4061/2011/864358.

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Chlorpromazine was used as a homogeneous electrocatalyst in the oxidation of captopril. The anodic peak current of chlorpromazine was increased substantially in the presence of low concentrations of captopril (pH 4). Cyclic voltammetry and chronoamperometry were used to study the kinetics of the catalytic electron transfer reaction. The values of electron transfer coefficient () and catalytic rate constant () were estimated to be 0.34 and , respectively. Linear sweep voltammetry was used for the determination of captopril in the presence of chlorpromazine. A linear calibration curve was obtain

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Amelia, Jesslyn, Yohanes Widodo Wirohadidjojo, and Agnes Sri Siswati. "The efficacy of captopril and 5-fluorouracil combination in the proliferation and collagen deposition of keloid fibroblast." Indonesian Journal of Biotechnology 27, no. 3 (2022): 126. http://dx.doi.org/10.22146/ijbiotech.69505.

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Keloid is a benign fibroproliferative tissue growth that exceeds the initial wound margins. Captopril has been tested in vitro to reduce fibroblast proliferation and collagen deposition; thus, it has potential for use in the treatment of keloids. Meanwhile, 5‐fluorouracil (5‐FU) has already been used in keloid management. This study aimed to determine the efficacy of the combination of captopril and 5‐FU in keloid fibroblast cultures. Keloid tissues were cultured up to passages 4–7. The study consisted of a control group, captopril in various concentrations (10‐2, 10‐3, 10‐4, and 10‐5 mol/L),

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Andreoli, S. P. "Captopril scavenges hydrogen peroxide and reduces, but does not eliminate, oxidant-induced cell injury." American Journal of Physiology-Renal Physiology 264, no. 1 (1993): F120—F127. http://dx.doi.org/10.1152/ajprenal.1993.264.1.f120.

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We investigated whether captopril, an angiotensin-converting enzyme (ACE) inhibitor with a sulfhydryl group, enalaprilat, an ACE inhibitor without a sulfhydryl group, and cysteine, an amino acid with a sulfhydryl group but no ACE-inhibiting properties, could scavenge hydrogen peroxide and prevent oxidant-induced cell injury. When 0.1-2.5 mM concentrations of captopril, cysteine, or enalaprilat were incubated with xanthine oxidase and hypoxanthine for 0-120 min, the recovery of hydrogen peroxide was significantly (P < 0.001) reduced in the presence of captopril or cysteine, whereas enalapril

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Zhang, Shaofeng, and Lin He. "Captopril reverses chronic unpredictable mild stress-induced depression-like behavior in rats via bradykinin-B2r signaling pathway." Tropical Journal of Pharmaceutical Research 21, no. 10 (2022): 2131–37. http://dx.doi.org/10.4314/tjpr.v21i10.13.

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Purpose: To investigate the effect of captopril on chronic unpredictable mild stress (CUMS)-induced depression-like behavior in mice, and the involvement of the bradykinin-B2r signaling pathway in the process.  Methods: Sixty healthy male C57BL/6J mice were assigned to control, model and high-, medium- and low-dose captopril groups and given the drug at doses of 9, 18 and 36 mg/kg, respectively. Open field and elevated cross maze tests were carried out, and escape latency in Morris water maze test was also test. The expressions of bradykinin B2R signal pathway proteins were assayed. &#x0

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&NA;. "Captopril." Reactions Weekly &NA;, no. 1393 (2012): 12. http://dx.doi.org/10.2165/00128415-201213930-00035.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 722 (1998): 7–8. http://dx.doi.org/10.2165/00128415-199807220-00012.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 727 (1998): 7. http://dx.doi.org/10.2165/00128415-199807270-00017.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 733 (1999): 7. http://dx.doi.org/10.2165/00128415-199907330-00010.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 1152 (2007): 8. http://dx.doi.org/10.2165/00128415-200711520-00024.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 1364 (2011): 12. http://dx.doi.org/10.2165/00128415-201113640-00044.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 535 (1995): 5. http://dx.doi.org/10.2165/00128415-199505350-00016.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 539 (1995): 5. http://dx.doi.org/10.2165/00128415-199505390-00007.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 546 (1995): 5. http://dx.doi.org/10.2165/00128415-199505460-00015.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 574 (1995): 5. http://dx.doi.org/10.2165/00128415-199505740-00012.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 583 (1996): 7. http://dx.doi.org/10.2165/00128415-199605830-00015.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 429 (1992): 6. http://dx.doi.org/10.2165/00128415-199204290-00023.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 433 (1993): 7. http://dx.doi.org/10.2165/00128415-199304330-00025.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 440 (1993): 7. http://dx.doi.org/10.2165/00128415-199304400-00024.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 443 (1993): 7. http://dx.doi.org/10.2165/00128415-199304430-00026.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 446 (1993): 7. http://dx.doi.org/10.2165/00128415-199304460-00025.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 451 (1993): 6. http://dx.doi.org/10.2165/00128415-199304510-00020.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 452 (1993): 6. http://dx.doi.org/10.2165/00128415-199304520-00024.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 457 (1993): 6. http://dx.doi.org/10.2165/00128415-199304570-00024.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 465 (1993): 6. http://dx.doi.org/10.2165/00128415-199304650-00022.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 471 (1993): 6. http://dx.doi.org/10.2165/00128415-199304710-00024.

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Brogden, Rex N., Peter A. Todd, and Eugene M. Sorkin. "Captopril." Drugs 36, no. 5 (1988): 540–600. http://dx.doi.org/10.2165/00003495-198836050-00003.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 610 (1996): 7. http://dx.doi.org/10.2165/00128415-199606100-00021.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 615 (1996): 7. http://dx.doi.org/10.2165/00128415-199606150-00015.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 682 (1997): 6–7. http://dx.doi.org/10.2165/00128415-199706820-00020.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 777 (1999): 7. http://dx.doi.org/10.2165/00128415-199907770-00011.

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&NA;. "Captopril." Reactions Weekly &NA;, no. 373 (1991): 4. http://dx.doi.org/10.2165/00128415-199103730-00015.

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