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Journal articles on the topic 'Ramiprilat'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Vree, Tom B., Erik Dammers, Ivan Ulc, Stefan Horkovics-Kovats, Miroslav Ryska, and IJsbrand Merkx. "Lack of Male-Female Differences in Disposition and Esterase Hydrolysis of Ramipril to Ramiprilat in Healthy Volunteers after a Single Oral Dose." Scientific World JOURNAL 3 (2003): 1344–58. http://dx.doi.org/10.1100/tsw.2003.122.

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The objective of this study was to identify differences in disposition and esterase hydrolysis of ramipril between male and female volunteers. Plasma concentration and area under the concentration-time curve until the last measured concentration (AUCt) data of ramipril and its active metabolite ramiprilat (-diacid) were obtained from a randomised, cross-over bioequivalence study in 36 subjects (18 females and 18 males). Participants received a single 5-mg oral dose of two different formulations of ramipril (Formulation I and II). Plasma ramipril and ramiprilat concentrations were determined ac

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2

Trobec, Katja Čvan, Iztok Grabnar, Jurij Trontelj, Mitja Lainščak, and Mojca Kerec Kos. "Population pharmacokinetics of ramipril in patients with chronic heart failure: A real-world longitudinal study." Acta Pharmaceutica 74, no. 2 (2024): 315–28. http://dx.doi.org/10.2478/acph-2024-0018.

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Abstract In patients with chronic heart failure (CHF), the use of angiotensin-converting enzyme inhibitors, including ramipril, is recommended to reduce the risk of heart failure worsening, hospitalisation, and death. Our aim was to investigate the influence of body composition on the pharmacokinetics of ramipril and its active metabolite ramiprilat and to evaluate the changes in pharmacokinetics after prolonged therapy. Twenty-three patients with CHF who were on regular therapy with ramipril participated at the first study visit ( median age 77 years, 65 % male, and 70 % New York Heart Associ

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3

M.Hareesh, Reddy* and Dr.A. Sambasiva Rao. "A COMPRAHENSIVE REVIEW OF PHARMACOLOGICAL AND THERAPEUTICAL ACTIVITIES OF ANTIHYPERTENSIVE DRUG RAMIPRIL." Indo American Journal of Pharmaceutical Sciences 04, no. 11 (2017): 3951–53. https://doi.org/10.5281/zenodo.1042737.

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Ramipril is an anti-hypertensive drug, a category of ACE inhibitor that inhibit the actions of angiotensin converting enzyme (ACE), thereby decreasing the production of angiotensin II and decreasing the breakdown of bradykinin. The decrease in an enzyme angiotensin II results in relaxation of arteriole smooth muscle leading to a lowering the total peripheral resistance, reducing blood pressure(BP) as the blood is pumped through widened. Ramipril, a precursor or prodrug, is converted to the active metabolite ramiprilat by carboxylesterase. It is mostly excreted by the kidneys. Its half-life is

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4

Khazaei, M., AM Sharifi, S. Golbidi, and I. Laher. "Reduction in Risk of Myocardial Infarction, Stroke, and Death from Cardiovascular Causes. Focus on Rampiril." Clinical Medicine. Therapeutics 1 (January 2009): CMT.S2095. http://dx.doi.org/10.4137/cmt.s2095.

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Several clinical studies demonstrate a beneficial role of angiotensin-converting enzyme (ACE) inhibitors in patients with myocardial infarction, hypertension and diabetes mellitus. This review focuses on the effects of ramipril, a weak inhibitor of ACE that is rapidly hydrolyzed to ramiprilat, an active metabolite. The Heart Outcome Prevention Evaluation (HOPE) study evaluated the effects of ramipril in patients with a high risk for cardiovascular events without pre-existing left ventricular dysfunction or heart failure. In this review, we summarized the effects of ramipril on myocardial infar

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5

Komers, R., and M. E. Cooper. "Acute renal hemodynamic effects of ACE inhibition in diabetic hyperfiltration: role of kinins." American Journal of Physiology-Renal Physiology 268, no. 4 (1995): F588—F594. http://dx.doi.org/10.1152/ajprenal.1995.268.4.f588.

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Angiotensin converting enzyme (ACE) inhibitors not only reduce angiotensin II (ANG II) levels but also inhibit kinin degradation. The relative roles of ANG II and bradykinin in the acute action of ACE inhibitors on renal hemodynamic parameters in rats after 3 wk of diabetes were explored using antagonists of the ANG II type 1 (AT1) and the bradykinin B2 receptors. Conscious control and streptozotocin diabetic male Sprague-Dawley rats were randomized to receive vehicle, the ACE inhibitor, ramiprilat, the B2-receptor blocker, HOE-140, the AT1-receptor blocker, valsartan, or the combination of ra

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6

DESMOULINS, P. O., S. BURGAUD, and L. J. I. HORSPOOL. "Pharmacokinetics and pharmacodynamics of ramipril and ramiprilat in healthy cats." Journal of Veterinary Pharmacology and Therapeutics 31, no. 4 (2008): 349–58. http://dx.doi.org/10.1111/j.1365-2885.2008.00959.x.

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7

A.B., Gangurde Mohammed Awais* V. A. Bairagi Abdurrahman Sanaurrehman Karishma Rajashri. "FORMULATION DEVELOPMENT AND IN VITRO EVALUATION OF FAST DISSOLVING TABLETS OF RAMIPRIL SOLID DISPERSION." INDO AMERICAN JOURNAL OF PHARMACEUTICAL SCIENCES 05, no. 08 (2018): 8409–16. https://doi.org/10.5281/zenodo.1411687.

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<em>Ramipril is a prodrug belonging to the angiotensin</em>-<em>converting enzyme </em>(<em>ACE</em>) <em>inhibitor which is metabolized to Ramiprilat in the liver and, to a lesser extent, kidneys</em>.<em>The poor solubility and wett</em> <em>ability of Ramipril leads to poor dissolution and variations in bioavailability</em>.<em>Solid dispersion of Ramipril was prepared using Hydroxy propyl β</em>- <em>cyclodextrin to improve water solubility</em>. <em>Prepared solid dispersion was shown improved solubility in water of 97</em>.<em>5 µg</em>/<em>ml</em>. <em>Fast dissolving tablets

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8

Skoglof, A., P. O. Göthe, and J. Deinum. "Effect of temperature and chloride on steady-state inhibition of angiotensin I-converting enzyme by enalaprilat and ramiprilat." Biochemical Journal 272, no. 2 (1990): 415–19. http://dx.doi.org/10.1042/bj2720415.

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The kinetics of the steady-state inhibition of angiotension I-converting enzyme (EC 3.4.15.1) at 25 degrees C and 37 degrees C with enalaprilat and ramiprilat can be simulated, assuming only one inhibitor-binding site, consistent with a 1:1 stoichiometry if the protein concentration was determined by amino acid analysis. In this temperature range the apparent inhibition constants for ramiprilat and enalaprilat were roughly doubled by a decrease in the chloride concentration from 0.300 M to 0.120 M.

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9

Chernonosov, Alexander. "The Use of Dried Blood Spots for the Quantification of Antihypertensive Drugs." International Journal of Analytical Chemistry 2018 (August 1, 2018): 1–12. http://dx.doi.org/10.1155/2018/3235072.

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Hypertension or high blood pressure is a harbinger of cardiovascular diseases. There are several classes of drugs used to treat hypertension. This review discusses the use of dried blood spots (DBSs) for the quantification by mass spectrometry (MS), tandem mass spectrometry (MS/MS), or, in some cases, by fluorescence detection methods the following antihypertensive medications: angiotensin-converting enzyme inhibitors (ramipril, ramiprilat, captopril, and lisinopril); angiotensin II receptor antagonists (valsartan, irbesartan, losartan, and losartan carboxylic acid); calcium channel blockers (

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10

Safari, Fatemeh, Sohrab Hajizadeh, Shahnaz Shekarforoush, Gholamreza Bayat, Mohsen Foadoddini, and Ali Khoshbaten. "Influence of ramiprilat and losartan on ischemia reperfusion injury in rat hearts." Journal of the Renin-Angiotensin-Aldosterone System 13, no. 1 (2011): 29–35. http://dx.doi.org/10.1177/1470320311426025.

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Hypothesis/introduction: Our aim was to investigate whether a non-hypotensive dose of ramiprilat and losartan has myocardial protective effects during myocardial ischemia/reperfusion in vivo. Materials and methods: Three groups of rats were given 10 mg/kg per day of losartan for one (L-1W), four (L-4W) or 10 (L-10W) weeks. Another three groups were given 50 µg/kg per day of ramiprilat for one (R-1W), four (R-4W) or 10 (R-10W) weeks. The animals underwent 30 min of left anterior descending artery occlusion and subsequent reperfusion for 120 min. Results: Myocardial infarct size (IS) was reduced

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11

Nordström, M., T. Abrahamsson, M. Ervik, E. Forshult, and C. G. Regårdh. "Central nervous and systemic kinetics of ramipril and ramiprilat in the conscious dog." Journal of Pharmacology and Experimental Therapeutics 266, no. 1 (1993): 147–52. https://doi.org/10.1016/s0022-3565(25)38308-4.

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12

Adler, Stephen, Harer Huang, Jean Noel Trochu, Xiaobin Xu, Shabnam Gupta, and Thomas H. Hintze. "Simvastatin reverses impaired regulation of renal oxygen consumption in congestive heart failure." American Journal of Physiology-Renal Physiology 281, no. 5 (2001): F802—F809. http://dx.doi.org/10.1152/ajprenal.00138.2001.

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First published July 12, 2001; 10.1152/ajprenal.00138.2001.—Nitric oxide (NO) production by endothelial nitric oxide synthase (eNOS) regulates renal O2consumption. This mechanism is impaired in heart and kidney of dogs with heart failure (CHF). Simvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase, increases eNOS expression in the endothelium. Therefore, we studied whether simvastatin treatment could restore the regulation of renal O2 consumption by stimulators of NO production in dogs with CHF. Renal O2consumption was measured after stimulation of NO production with bradykinin

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13

Serrano-Rodríguez, J. M., M. Gómez-Díez, M. Esgueva, et al. "Pharmacokinetics and pharmacodynamics of ramipril and ramiprilat after intravenous and oral doses of ramipril in healthy horses." Veterinary Journal 208 (February 2016): 38–43. http://dx.doi.org/10.1016/j.tvjl.2015.10.024.

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14

Forfia, Paul R., Xiaoping Zhang, Delvin R. Knight, et al. "NO modulates myocardial O2consumption in the nonhuman primate: an additional mechanism of action of amlodipine." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (1999): H2069—H2075. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h2069.

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Recent evidence from our laboratory and others suggests that nitric oxide (NO) is a modulator of in vivo and in vitro oxygen consumption in the murine and canine heart. Therefore, the goal of our study was twofold: to determine whether NO modulates myocardial oxygen consumption in the nonhuman primate heart in vitro and to evaluate whether the seemingly cardioprotective actions of amlodipine may involve an NO-mediated mechanism. Using a Clark-type O2 electrode, we measured oxygen consumption in cynomologous monkey heart at baseline and after increasing doses of S-nitroso- N-acetylpenicillamine

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15

Rump, A. F. E., D. Koreuber, R. Rösen, and W. Klaus. "Cardioprotection by ramiprilat in isolated rabbit hearts." European Journal of Pharmacology 241, no. 2-3 (1993): 201–7. http://dx.doi.org/10.1016/0014-2999(93)90204-u.

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16

Gupta, V. K., Rajeev Jain, Ojitkumar Lukram, Shilpi Agarwal, and Ashish Dwivedi. "Simultaneous determination of ramipril, ramiprilat and telmisartan in human plasma using liquid chromatography tandem mass spectrometry." Talanta 83, no. 3 (2011): 709–16. http://dx.doi.org/10.1016/j.talanta.2010.10.011.

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17

Yuan, Bo, Xuan Wang, Fenge Zhang, Jun Jia, and Fangling Tang. "Simultaneous Determination of Ramipril and Its Active Metabolite Ramiprilat in Human Plasma by LC–MS–MS." Chromatographia 68, no. 7-8 (2008): 533–39. http://dx.doi.org/10.1365/s10337-008-0757-5.

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18

Grafe, M., C. Bossaller, K. Graf, et al. "Effect of angiotensin-converting-enzyme inhibition on bradykinin metabolism by vascular endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 5 (1993): H1493—H1497. http://dx.doi.org/10.1152/ajpheart.1993.264.5.h1493.

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The degradation of bradykinin by angiotensin-converting-enzyme (ACE) activity in cultured human endothelial cells was studied by direct measurement of bradykinin and by its effect on the release of endothelium-derived relaxing factors. The half-life of exogenous bradykinin (10,000 pg/ml) was calculated from the decay of the bradykinin concentration as 46 +/- 2 min in cell monolayers, 133 +/- 15 min in conditioned medium, and 24 +/- 2 min in homogenates. Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisi

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19

Regulska, Katarzyna, Joanna Musiał, and Beata J. Stanisz. "Solid-State Stability Profiling of Ramipril to Optimize Its Quality Efficiency and Safety." Pharmaceutics 13, no. 10 (2021): 1600. http://dx.doi.org/10.3390/pharmaceutics13101600.

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High global expenditure on out-of-label-date drugs, along with safety concerns associated with the accumulation of degradation impurities, justify the need for stability profiling. In this article, a comprehensive study on the solid-state stability of ramipril (RAM) was performed via isothermal methods under stress conditions. A validated stability-indicating HPLC protocol was used. The effects of various factors on the rate of RAM degradation were investigated, including: temperature, relative air humidity (RH), excipients (talc, starch, methylcellulose and hydroxypropyl methylcellulose), mod

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20

Zhu, Zhimeng, Andre Vachareau, and Len Neirinck. "Liquid chromatography–mass spectrometry method for determination of ramipril and its active metabolite ramiprilat in human plasma." Journal of Chromatography B 779, no. 2 (2002): 297–306. http://dx.doi.org/10.1016/s1570-0232(02)00398-7.

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21

Bünning, Peter. "Kinetic Properties of the Angiotensin Converting Enzyme Inhibitor Ramiprilat." Journal of Cardiovascular Pharmacology 10 (1987): 31–35. http://dx.doi.org/10.1097/00005344-198706107-00005.

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22

Baumgarten, Claus R., Wolfgang Linz, Gert Kunkel, Bernward A. Schölkens, and Gabriele Wiemer. "Ramiprilat increases bradykinin outflow from isolated hearts of rat." British Journal of Pharmacology 108, no. 2 (1993): 293–95. http://dx.doi.org/10.1111/j.1476-5381.1993.tb12797.x.

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23

Hartman, J. Craig, Theron M. Wall, Thomas G. Hullinger, and Ronald J. Shebuski. "Reduction of Myocardial Infarct Size in Rabbits by Ramiprilat." Journal of Cardiovascular Pharmacology 21, no. 6 (1993): 996–1003. http://dx.doi.org/10.1097/00005344-199306000-00022.

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24

Albus, Udo, Ingeborg Kress, Wolfgang Linz, Daniel Vasmant, Françoise Delarue, and Jean-Daniel Sraer. "High affinity binding of ramiprilat on isolated human glomeruli." Biochemical Pharmacology 37, no. 24 (1988): 4679–84. http://dx.doi.org/10.1016/0006-2952(88)90337-1.

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25

Lefebvre, Hervé P., Elisabeth Jeunesse, Valérie Laroute, and Pierre-Louis Toutain. "Pharmacokinetic and Pharmacodynamic Parameters of Ramipril and Ramiprilat in Healthy Dogs and Dogs with Reduced Glomerular Filtration Rate." Journal of Veterinary Internal Medicine 20, no. 3 (2006): 499–507. http://dx.doi.org/10.1111/j.1939-1676.2006.tb02888.x.

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26

Hartman, J. C., G. M. Kurc, T. G. Hullinger, T. M. Wall, R. M. Sheehy, and R. J. Shebuski. "Inhibition of nitric oxide synthase prevents myocardial protection by ramiprilat." Journal of Pharmacology and Experimental Therapeutics 270, no. 3 (1994): 1071–76. https://doi.org/10.1016/s0022-3565(25)22498-3.

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27

Kalinowski, Marc, Gunnar Tepe, Andrea Schieber, et al. "Local Administration of Ramiprilat is Less Effective than Oral Ramipril in Preventing Restenosis after Balloon Angioplasty in an Animal Model." Journal of Vascular and Interventional Radiology 10, no. 10 (1999): 1397–404. http://dx.doi.org/10.1016/s1051-0443(99)70251-4.

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28

Paulus, E. F., R. Henning, and H. Urbach. "Structure of the angiotensin-converting enzyme inhibitor ramiprilat (HOE 498 diacid)." Acta Crystallographica Section C Crystal Structure Communications 43, no. 5 (1987): 941–45. http://dx.doi.org/10.1107/s0108270187093491.

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29

Hong, Young Joon, Myung Ho Jeong, Jung Ha Kim, et al. "EFFECT OF RAMIPRILAT-COATED STENT IN A PORCINE CORONARY RESTENOSIS MODEL." Journal of the American College of Cardiology 55, no. 10 (2010): A166.E1555. http://dx.doi.org/10.1016/s0735-1097(10)61556-2.

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30

HARTMAN, J. "Role of bradykinin in reduction of myocardial infarct size by ramiprilat." Journal of Molecular and Cellular Cardiology 24 (June 1992): S11. http://dx.doi.org/10.1016/0022-2828(92)92889-k.

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31

Dendorfer, Andreas, Siegmund Reiβmann, Sebastian Wolfrum, Walter Raasch, and Peter Dominiak. "Potentiation of Kinin Analogues by Ramiprilat Is Exclusively Related to Their Degradation." Hypertension 38, no. 1 (2001): 142–46. http://dx.doi.org/10.1161/01.hyp.38.1.142.

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32

Wiemer, G., B. A. Schölkens, R. H. Becker, and R. Busse. "Ramiprilat enhances endothelial autacoid formation by inhibiting breakdown of endothelium-derived bradykinin." Hypertension 18, no. 4 (1991): 558–63. http://dx.doi.org/10.1161/01.hyp.18.4.558.

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33

Martorana, P. A., W. Linz, B. Kettenbach, and B. A. Schölkens. "Bradykinin and the ace-inhibitor ramiprilat reduce inffarct-size in die dog." European Journal of Pharmacology 183, no. 2 (1990): 205. http://dx.doi.org/10.1016/0014-2999(90)93041-n.

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34

Martorana, P. A., H. Ruetten, B. Goebel, et al. "Ramiprilat prevents the development of acute coronary endothelial dysfunction in the dog." Basic Research in Cardiology 94, no. 4 (1999): 238–45. http://dx.doi.org/10.1007/s003950050148.

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35

Persson, Bengt-Arne, Christina Fakt, Magnar Ervik, and Martin Ahnoff. "Interference from a glucuronide metabolite in the determination of ramipril and ramiprilat in human plasma and urine by gas chromatography–mass spectrometry." Journal of Pharmaceutical and Biomedical Analysis 40, no. 3 (2006): 794–98. http://dx.doi.org/10.1016/j.jpba.2005.08.013.

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36

Tan, Aimin, Wen Jin, Fu Deng, Saleh Hussain, Adrien Musuku, and Robert Massé. "Bioanalytical method development and validation using incurred samples—Simultaneous quantitation of ramipril and ramiprilat in human EDTA plasma by LC–MS/MS." Journal of Chromatography B 877, no. 29 (2009): 3673–80. http://dx.doi.org/10.1016/j.jchromb.2009.09.017.

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37

Baudin, B., and L. Drouet. "In Vitro Interactions Between Ramiprilat and Angiotensin I-Converting Enzyme in Endothelial Cells." Journal of Cardiovascular Pharmacology 14, no. 4 (1989): S37—S42. http://dx.doi.org/10.1097/00005344-198900000-00009.

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38

Becker, R. H. A., U. Albus, I. Kress, et al. "High-Affinity Binding of the Converting Enzyme Inhibitor, Ramiprilat, to Isolated Human Glomeruli." Journal of Cardiovascular Pharmacology 13 (1989): S31—S34. http://dx.doi.org/10.1097/00005344-198900133-00008.

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39

Baudin, B., and L. Drouet. "In Vitro Interactions Between Ramiprilat and Angiotensin I-Converting Enzyme in Endothelial Cells." Journal of Cardiovascular Pharmacology 14 (1989): S37—S42. http://dx.doi.org/10.1097/00005344-198906144-00009.

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40

Chen, K., and B. G. Zimmerman. "Comparison of renal hemodynamic effect of ramiprilat to captopril; possible role of kinins." Journal of Pharmacology and Experimental Therapeutics 270, no. 2 (1994): 491–97. https://doi.org/10.1016/s0022-3565(25)22408-9.

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41

Cachofeiro, V., T. Sakakibara, and A. Nasjletti. "Kinins, nitric oxide, and the hypotensive effect of captopril and ramiprilat in hypertension." Hypertension 19, no. 2 (1992): 138–45. http://dx.doi.org/10.1161/01.hyp.19.2.138.

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42

LINZ, W., P. PETRY, B. SCHOLKENS, and P. MARTORANA. "Ramiprilat and nicainoprol reduce reperfusion arrhythmias in the isolated ischemic working rat heart." Journal of Molecular and Cellular Cardiology 18 (1986): 23. http://dx.doi.org/10.1016/s0022-2828(86)80368-6.

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43

Pi, X. "Captopril and ramiprilat protect against free radical injury in isolated working rat hearts." Journal of Molecular and Cellular Cardiology 21, no. 12 (1989): 1261–71. http://dx.doi.org/10.1016/0022-2828(89)90672-x.

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44

Wall, Theron M., Daniel A. Linseman, and J. Craig Hartman. "Ramiprilat attenuates hypoxia/reoxygenation injury to cardiac myocytes via a bradykinin-dependent mechanism." European Journal of Pharmacology 306, no. 1-3 (1996): 165–74. http://dx.doi.org/10.1016/0014-2999(96)00030-1.

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45

Minshall, R. D., V. P. Yelamanchi, A. Djokovic, et al. "Importance of sympathetic innervation in the positive inotropic effects of bradykinin and ramiprilat." Circulation Research 74, no. 3 (1994): 441–47. http://dx.doi.org/10.1161/01.res.74.3.441.

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46

Zegner, M., B. Podesser, G. Koci, et al. "Bewertung der Reperfusion unter Einfluß von Ramiprilat—Untersuchungen am isolierten «Working-heart-Modell»." European Surgery 28, no. 6 (1996): 343–46. http://dx.doi.org/10.1007/bf02616280.

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47

Hong, Young Joon, Myung Ho Jeong, Jung Ha Kim, et al. "AS-103: Effect of Ramiprilat-Coated Stent in a Porcine Coronary Restenosis Model." American Journal of Cardiology 103, no. 9 (2009): 46B—47B. http://dx.doi.org/10.1016/j.amjcard.2009.01.152.

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48

Baudin, Bruno, and BÉNÉDicte Bénéteau-Burnat. "Mixed-Type Inhibition of Pulmonary Angiotensin I-Converting Enzyme by Captopril, Enalaprilat and Ramiprilat." Journal of Enzyme Inhibition 14, no. 6 (1999): 447–56. http://dx.doi.org/10.3109/14756369909030335.

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49

Linz, Wolfgang, Udo Albus, and Bernward A. Schölkens. "Effects of endothelin on isolated ischaemic rat hearts during ramiprilat, bradykinin and indomethacin perfusion." Journal of Hypertension 7 (1989): S310–311. http://dx.doi.org/10.1097/00004872-198900076-00151.

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50

Helmig, S., P. Schuckenböhmer, J. Heger, G. Euler, H. M. Piper, and K. D. Schlüter. "Direct effects of the angiotensin-converting enzyme inhibitor ramiprilat on adult rat ventricular cardiomyocytes." Acta Physiologica 191, no. 4 (2007): 267–74. http://dx.doi.org/10.1111/j.1748-1716.2007.01738.x.

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