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Journal articles on the topic 'Felodipine'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

Van Hamersvelt, H. W., J. F. Wetzels, H. J. Kloke, R. A. Koene, and F. T. Huysmans. "Exogenous aldosterone antagonizes distal tubular effects of calcium entry blocker felodipine." American Journal of Physiology-Renal Physiology 266, no. 6 (June 1, 1994): F843—F849. http://dx.doi.org/10.1152/ajprenal.1994.266.6.f843.

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Calcium entry blockers, such as felodipine, increase natriuresis without increasing kaliuresis. Since these drugs acutely increase plasma renin activity without a concomitant change of aldosterone, inhibition of such stimulated aldosterone release might explain the absence of kaliuresis. In a randomized crossover study in 12 male volunteers, we compared the effects of simultaneously administered exogenous aldosterone and felodipine with the effects of either felodipine or aldosterone alone. Felodipine infusion decreased blood pressure, increased renal plasma flow, and induced natriuresis without kaliuresis. Aldosterone alone reduced sodium excretion and increased potassium excretion without influencing hemodynamics. Addition of aldosterone to felodipine attenuated its natriuretic effect and induced a kaliuresis, which clearly exceeded the rise of potassium excretion during aldosterone alone [delta% fractional excretion of K+ +42 +/- 12 with felodipine+aldosterone and +7 +/- 8% with aldosterone alone; means +/- SE, P < 0.02]. Our data suggest that felodipine-mediated inhibition of stimulated aldosterone release is essential for the absence of kaliuresis with felodipine. In addition, the pronounced kaliuresis with aldosterone during felodipine is in keeping with increased distal sodium delivery due to a proximal tubular action of felodipine.

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2

&NA;. "Felodipine." Reactions Weekly &NA;, no. 1078 (November 2005): 12. http://dx.doi.org/10.2165/00128415-200510780-00030.

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3

&NA;. "Felodipine." Reactions Weekly &NA;, no. 1047 (April 2005): 10. http://dx.doi.org/10.2165/00128415-200510470-00028.

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4

&NA;. "Felodipine." Reactions Weekly &NA;, no. 700 (May 1998): 8. http://dx.doi.org/10.2165/00128415-199807000-00025.

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5

&NA;. "Felodipine." Reactions Weekly &NA;, no. 716 (August 1998): 8. http://dx.doi.org/10.2165/00128415-199807160-00027.

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6

&NA;. "Felodipine." Reactions Weekly &NA;, no. 1289 (February 2010): 19. http://dx.doi.org/10.2165/00128415-201012890-00058.

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7

Faulds, Diana, and Eugene M. Sorkin. "Felodipine." Drugs & Aging 2, no. 5 (1992): 374–88. http://dx.doi.org/10.2165/00002512-199202050-00002.

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8

&NA;. "Felodipine." Reactions Weekly &NA;, no. 872 (October 2001): 8–9. http://dx.doi.org/10.2165/00128415-200108720-00024.

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9

Saltiel, E., A. Gray Ellrodt, Jon P. Monk, and Mark S. Langley. "Felodipine." Drugs 36, no. 4 (October 1988): 387–428. http://dx.doi.org/10.2165/00003495-198836040-00002.

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10

Todd, Peter A., and Diana Faulds. "Felodipine." Drugs 44, no. 2 (August 1992): 251–77. http://dx.doi.org/10.2165/00003495-199244020-00008.

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11

&NA;. "Felodipine." Reactions Weekly &NA;, no. 375 (November 1991): 7. http://dx.doi.org/10.2165/00128415-199103750-00034.

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12

Kvachakhiya, L. L., V. K. Shormanov, and N. S. Kononenko. "Determination of felodipine in biological fluids." Kazan medical journal 100, no. 4 (July 31, 2019): 650–56. http://dx.doi.org/10.17816/kmj2019-650.

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Aim. Development of methods for the determination of felodipine in blood and plasma. Methods. The study object was felodipine [3-ethyl-5-methyl-4-(2,3-dichlorophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylate]. The experiments were carried out on model mixtures of felodipine with blood and human blood plasma. Acetone was proposed as an isolating agent for the extraction of felodipine from biological fluids. To identify and quantify felodipine in extracts from blood and plasma, the methods of thin-layer chromatography, spectrophotometry and gas-liquid chromatography in combination with mass spectrometry were proposed. Results. The possibility of using acetone as an isolating agent to extract felodipine from biological fluids is demonstrated. The optimal conditions for the extraction of felodipine with acetone were found to be achieved already at 2-fold infusion of a biological object with an isolating agent, if the mass ratio of isolating liquid and biological material at each infusion stage is at least 2:1, and the infusion time is at least 30 minutes. Optimal felodipine purification conditions were achieved in a macrocolumn (15×1 cm) of Silasorb S-18 sorbent of 30 μm with elution of the substance with the polar eluent acetonitrile-water (7:3). The methods of determining felodipine in the blood and plasma were developed. With the content of felodipine of 25 mg in 25 g of biological fluid, the developed methods allow determining 86.01–87.86% in blood and 95.64–96.18% of the substance in blood plasma. The values of the detection limit of felodipine in the blood and plasma by the developed methods are 200 μg/100 g and 150 μg/100 g, respectively. Conclusion. Methods for the determination of felodipine in biological fluids were developed based on isolating with acetone and purification in the Silasorb S-18 sorbent column; use of these methods allows determining up to 87.86% of the analyte in the blood and up to 96.18% in the blood plasma.

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13

Katzman, Per L., U. Lennart Hulthén, and Bernt Hökfelt. "Glucoregulatory hormone response to insulin-induced hypoglycaemia following long-term calcium antagonism with felodipine in patients with essential hypertension." Acta Endocrinologica 116, no. 4 (December 1987): 473–78. http://dx.doi.org/10.1530/acta.0.1160473.

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Abstract. The effect of 8 weeks' treatment with the dihydropyridine calcium antagonist felodipine on glucoregulatory hormone response following insulin-induced hypoglycaemia was evaluated in 7 patients with essential hypertension, WHO grade I–II. After an iv insulin injection (0.1 IU/kg), blood glucose decrement and nadir were similar before and during felodipine treatment. Basal glucagon, noradrenaline, adrenaline, GH and cortisol levels were unchanged, and the response to insulin-induced hypoglycaemia was similar before and during felodipine treatment. Basal plasma dopamine levels were similar and did not change during insulin-induced hypoglycaemia before and during felodipine treatment. Basal serum levels of TSH, T3 and T4 were unaltered following felodipine. In conclusion, long-term treatment with felodipine did not alter the hypoglycaemic effect of exogenous insulin, or the recovery from hypoglycaemia or the glucoregulatory hormone response to insulin-induced hypoglycaemia in patients with essential hypertension.

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14

Solanko, Katarzyna A., Artem O. Surov, German L. Perlovich, Annette Bauer-Brandl, and Andrew D. Bond. "Felodipine–diazabicyclo[2.2.2]octane–water (1/1/1)." Acta Crystallographica Section C Crystal Structure Communications 68, no. 11 (October 31, 2012): o456—o458. http://dx.doi.org/10.1107/s0108270112043405.

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The title compound, C18H19Cl2NO4·C6H12N2·H2O, is a cocrystal hydrate containing the active pharmaceutical ingredient felodipine and diazabicyclo[2.2.2]octane (DABCO). The DABCO and water molecules are linked through O—H...N hydrogen bonds into chains around 21screw axes, while the felodipine molecules form N—H...O hydrogen bonds to the water molecules. The felodipine molecules adopt centrosymmetric back-to-back arrangements that are similar to those present in all of its four reported polymorphs. The dichlorophenyl rings also form π-stacking interactions. The inclusion of water molecules in the cocrystal, rather than formation of N—H...N hydrogen bonds between felodipine and DABCO, may be associated with steric hindrance that would arise between DABCO and the methyl groups of felodipine if they were directly involved in hydrogen bonding.

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15

&NA;. "Felodipine overdose." Reactions Weekly &NA;, no. 1266 (August 2009): 18. http://dx.doi.org/10.2165/00128415-200912660-00055.

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16

&NA;. "Amlodipine/felodipine." Reactions Weekly &NA;, no. 1312 (July 2010): 9–10. http://dx.doi.org/10.2165/00128415-201013120-00029.

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17

Haria, Malini, Greg L. Plosker, and Anthony Markham. "Felodipine/Metoprolol." Drugs 59, no. 1 (January 2000): 141–57. http://dx.doi.org/10.2165/00003495-200059010-00011.

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18

&NA;. "Felodipine interaction." Reactions Weekly &NA;, no. 565 (August 1995): 7. http://dx.doi.org/10.2165/00128415-199505650-00025.

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19

&NA;. "Felodipine/nifedipine." Reactions Weekly &NA;, no. 736 (January 1999): 8. http://dx.doi.org/10.2165/00128415-199907360-00023.

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20

&NA;. "Felodipine interaction." Reactions Weekly &NA;, no. 1009 (July 2004): 9. http://dx.doi.org/10.2165/00128415-200410090-00025.

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21

&NA;. "Felodipine ER." Drugs & Therapy Perspectives 1, no. 3 (February 1993): 1–4. http://dx.doi.org/10.2165/00042310-199301030-00001.

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22

&NA;. "Felodipine interaction." Reactions Weekly &NA;, no. 370 (September 1991): 6. http://dx.doi.org/10.2165/00128415-199103700-00022.

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23

Harvengt, C. "Felodipine – Olsalazine." Acta Clinica Belgica 44, no. 2 (January 1989): 137–39. http://dx.doi.org/10.1080/17843286.1989.11718002.

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24

&NA;. "Felodipine/sorafenib." Reactions Weekly &NA;, no. 1395 (March 2012): 22. http://dx.doi.org/10.2165/00128415-201213950-00073.

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25

V, Kishan, Usha Kiranmai Gondrala, and Narendar Dudhipala. "Preparation, Characterization and in vivo Evaluation of Felodipine Solid-Lipid Nanoparticles for Improved Oral Bioavailability." International Journal of Pharmaceutical Sciences and Nanotechnology 8, no. 4 (November 30, 2015): 2995–3002. http://dx.doi.org/10.37285/ijpsn.2015.8.4.1.

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Felodipine is an antihypertensive drug with poor oral bioavailability due to the first pass metabolism. For improving the oral bioavailability, felodipine loaded solid lipid nanoparticles (SLNs) were developed using trimyristin, tripalmitin and glyceryl monostearate. Poloxamer 188 was used as surfactant. Lipid excipient compatibilities were confirmed by differential scanning calorimetry. SLN dispersions were prepared by hot homogenization of molten lipids and aqueous phase followed by ultrasonication at a temperature, above the melting point. SLNs were characterized for particle size, zeta potential, drug content, entrapment efficiency and crystallinity of lipid and drug. In vitro release studies were performed in 0.1N HCl and phosphate buffer of pH 6.8 using dialysis method. Pharmacokinetics of felodipine-SLNs after oral admini-stration in male Wistar rats was studied. The bioavailability of felodipine was increased by 1.75 fold when compared to that of a felodipine suspension.

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26

Liu, Yuefei, Alexandra Opitz-Gress, Albert Rott, Florian Liewald, Ludger Sunder-Plassmann, Manfred Lehmann, Martin Stauch, and Jürgen M. Steinacker. "Effect of Felodipine on Regional Blood Supply and Collateral Vascular Resistance in Patients with Peripheral Arterial Occlusive Disease." Vascular Medicine 2, no. 1 (February 1997): 13–18. http://dx.doi.org/10.1177/1358863x9700200103.

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This double-blinded, randomized, placebo-controlled study was designed to investigate the acute effect of felodipine on regional blood supply and collateral vascular resistance in patients with peripheral arterial occlusive disease (PAOD). Thirty men with PAOD were treated with a single dose of 5 mg felodipine or placebo. Systolic blood pressure (SBP), Doppler ankle pressure (DAP), calf blood flow (CBF) by venous occlusion plethysmography and calf transcutaneous oxygen tension (tc pO2) were measured during a cycle ergometry. Felodipine reduced SBP significantly (from 149 to 136 mmHg, p < 0.05), while placebo did not. DAP increased slightly but not significantly in both groups. The pressure gradient between SBP and DAP fell significantly in the felodipine group (60 vs 39 mmHg, p < 0.01) but not in the placebo group (59 vs 56 mmHg). There was a trend for lower velocity in tc pO2 decrease during the stress test and higher velocity of tc pO2 increase during recovery from exercise in the felodipine group although the differences between both groups were not significant. In the felodipine group, CBF increased by 35.6% ( p < 0.05) whereas it did not change in the placebo group. In conclusion, while lowering SBP, felodipine increased slightly, or at least maintained, the blood supply to the calves in PAOD patients, which probably results from reducing collateral vascular resistance.

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27

Wang, Bing-Yin, Josef Niebauer, Alan H. Singer, Philip S. Tsao, and John P. Cooke. "Felodipine Inhibits Intimal Lesion Formation in the Hypercholesterolemic Rabbit: Differential Effects on Endothelial and Monocyte Determinants of Atherogenesis." Vascular Medicine 1, no. 3 (August 1996): 173–79. http://dx.doi.org/10.1177/1358863x9600100301.

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The purpose of this study was to determine if the calcium entry antagonist felodipine inhibited intimal lesion formation in hypercholesterolemic rabbits, and to determine if this was due to an effect upon monocyte and/or endothelial determinants of this interaction. Twenty-three male New Zealand White rabbits received the following treatment regimen for 10 weeks: normal chow (NP, n = 3); normal chow with felodipine infusion (NF, n=6); 0.5% cholesterol chow (CP, n = 7); or 0.5% cholesterol chow and felodipine infusion (CF, n=7). After 10 weeks blood was collected for biochemical measurements and mononuclear cell binding assays, and thoracic aortae were harvested for vascular reactivity studies and histomorphometry. In the animals receiving normal chow, felodipine did not significantly affect blood pressure, plasma cholesterol levels, binding studies, vascular reactivity, or structure; therefore these animals were analyzed as one group (N). Plasma cholesterol levels were significantly elevated in groups receiving the 0.5% cholesterol diet (N, 29±3 mg/dl; CP, 1221±73 mg/dl; CF, 979±108 mg/dl). High-density lipoprotein cholesterol was not different between the groups (25±4 vs 23±4 vs 27±4 mg/dl; N vs CF vs CP respectively; p=NS). Cholesterol feeding markedly augmented the adhesiveness of mononuclear cells, as demonstrated by a 250% increase in cell binding. Felodipine did not alter the adhesiveness of mononuclear cells in hypercholesterolemic animals. Cholesterol feeding significantly impaired endothelium-dependent relaxations. Endothelium-dependent relaxations were restored by felodipine treatment as reflected by the maximal responses to acetylcholine (40±7% vs 58±4% vs 67±5%; CP vs CF vs N respectively). The improvement in endothelium-dependent relaxation in the felodipine-treated animals was associated with a 2.2-fold reduction in lesion surface area of the thoracic aorta (8.2±6.3% vs 18.2±9.5%; CF vs CP; p<0.01). Moreover, the intima/media ratio reflecting lesion thickness was substantially reduced by felodipine treatment (0.05±0.02 vs 0.20±0.07; CF vs CP; p=0.006). Ex vivo studies revealed that felodipine inhibited the adhesiveness of vascular endothelium, but not mononuclear cells, derived from hypercholesterolemic animals. Low-dose felodipine appears to inhibit monocyte-endothelial interaction, as indicated by a reduction in the formation of lesions in hypercholesterolemic animals. This effect is not due to an alteration in adhesiveness of mononuclear cells. The salutary effect of felodipine is associated with an increase in vascular nitric oxide activity which may reduce endothelial adhesiveness.

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28

Iovanov, Rareș Iuliu, Ioan Tomuță, and Sorin Emilian Leucuța. "Development of a reservoir type prolonged release system with felodipine via simplex methodology." Medicine and Pharmacy Reports 89, no. 1 (September 28, 2015): 128–36. http://dx.doi.org/10.15386/cjmed-526.

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Background and aims. Felodipine is a dihydropyridine calcium antagonist that presents good characteristics to be formulated as prolonged release preparations. The aim of the study was the formulation and in vitro characterization of a reservoir type prolonged release system with felodipine, over a 12 hours period using the Simplex method.Methods. The first step of the Simplex method was to study the influence of the granules coating method on the felodipine release. Furthermore the influence of the coating polymer type, the percent of the coating polymer and the percent of pore forming agent in the coating on the felodipine release were studied. Afterwards these two steps of the experimental design the percent of Surelease applied on the felodipine loaded granules and the percent of pore former in the polymeric coating formulation variables were studied. The in vitro dissolution of model drug was performed in phosphate buffer solution (pH 6.5) with 1% sodium lauryl sulfate. The released drug quantification was done using an HPLC method. The release kinetics of felodipine from the final granules was assessed using different mathematical models.Results. A 12 hours release was achieved using granules with the size between 315 – 500 µm coated with 45% Surelease with different pore former ratios in the coating via the top-spray method.Conclusion. We have prepared prolonged release coated granules with felodipine using a fluid bed system based on the Simplex method. The API from the studied final formulations was released over a 12 hours period and the release kinetics of the model drug substance from the optimized preparations fitted best the Higuchi and Peppas kinetic models.

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29

Wei, Chiming, and John C. Burnett. "Inhibition by calcium antagonism of circulating and renal endothelin in experimental congestive heart failure." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 1 (January 1, 2000): H263—H268. http://dx.doi.org/10.1152/ajpheart.2000.278.1.h263.

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Endothelin (ET) is a potent vasoconstrictor and sodium-regulating peptide whose tissue and plasma concentrations are increased in congestive heart failure (CHF). ET may mediate its vasoconstrictor and sodium-regulatory actions secondary to an increase in intracellular calcium. Calcium influx may augment ET synthesis. Although felodipine, a dihydropyridine calcium-channel antagonist, is effective in reducing vascular resistance in generalized vasoconstriction, its actions in CHF on circulating and local tissue ET remain undefined. The current studies were designed to determine the modulating actions of felodipine (oral, 40 mg/day for 7 days; n= 6) in an experimental canine model of CHF produced by chronic thoracic inferior vena caval constriction (TIVCC) compared with normal ( n = 7) and TIVCC-alone ( n = 7) dogs. We hypothesized that felodipine would decrease circulating and renal ET. Plasma ET was significantly increased in TIVCC compared with normal dogs (26 ± 0.5 vs. 12 ± 0.7 pg/ml, P < 0.05) and was markedly decreased by felodipine compared with TIVCC alone (14 ± 3 vs. 26 ± 0.5 pg/ml, P < 0.05). Renal ET immunohistochemical staining demonstrated the presence of ET in normal kidney, which was markedly increased in renal cortex and medulla in TIVCC dogs. Renal cortical and medullary ET staining densities were markedly decreased with felodipine compared with those with TIVCC alone. In the TIVCC + felodipine group, cardiovascular hemodynamics also was markedly improved compared with the TIVCC-alone group [systemic vascular resistance: 27 ± 2 vs. 44 ± 3 resistance units (RU), P < 0.05; pulmonary vascular resistance: 3.3 ± 0.1 vs. 5.7 ± 0.4 RU, P < 0.05; cardiac output: 2.9 ± 0.2 vs. 1.7 ± 0.1 l/min, P < 0.05]. This study demonstrates important modulating inhibitory actions of felodipine on renal and plasma ET in an experimental model of CHF.

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30

Dunselman, Peter H. J. M., and Boo Edgar. "Felodipine Clinical Pharmacokinetics." Clinical Pharmacokinetics 21, no. 6 (December 1991): 418–30. http://dx.doi.org/10.2165/00003088-199121060-00003.

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31

Liedholm, Hans, and Gunnar Nordin. "Erythromycin-Felodipine Interaction." DICP 25, no. 9 (September 1991): 1007–8. http://dx.doi.org/10.1177/106002809102500918.

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32

Kennerfalk, Anita, Per Lundborg, and Mari-Ann Wallander. "Felodipine Safety Evaluation." Journal of Cardiovascular Pharmacology 15, Supplement 4 (1990): S106. http://dx.doi.org/10.1097/00005344-199015004-00034.

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33

Mace, P. J. E., T. J. Stallard, and W. A. Littler. "Felodipine in hypertension." European Journal of Clinical Pharmacology 29, no. 4 (1985): 383–89. http://dx.doi.org/10.1007/bf00613449.

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34

Thanh, Duyen Nguyen Thi, Duc Hoang Van, Minh Vo Xuan, Xuan Dam Thanh Thanh, and Tung Bui Thanh. "Design and Optimization of Hydrophilic Matrix-based Sustained Release Felodipine Tablets." International Journal of Pharmaceutical Sciences and Nanotechnology 11, no. 3 (May 31, 2018): 4136–44. http://dx.doi.org/10.37285/ijpsn.2018.11.3.8.

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Felodipine is a calcium channel blocker used for hypertensive and unstable angina treatments. The sustained release formulations of felodipine have advantages of achieving good therapeutic effects, increasing the bioavailability, decreasing dosing times per day and reducing side effects.The aim of our study was to study the formulation screening, then use an experiment design for formulating a hydrophilic matrix sustained release tablet of felodipine. Methods: The optimization process had the influences of the chosen excipients (including HPMC E4M, HPMC E15LV) on the drug release. Three dependent variables were percentages of released felodipine at the sampling times 2h, 6h, 10h (Y2, Y6, Y10, respectively). Results: The release profile from the optimized formula almost met the predicted release profile and was similar to reference tablets. The kinetics of drug release the optimized tablets and reference tablets were also followed the Korsmeyer – Peppas model.Conclusion: The optimized formula was obtained, and the in vitro release profile was similar to the predicted profile and reference tablets.

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35

Liau, CS, KL Chien, CL Chao, and TM Lee. "Efficacy and Safety of Barnidipine Compared with Felodipine in the Treatment of Hypertension in Chinese Patients." Journal of International Medical Research 30, no. 3 (June 2002): 330–36. http://dx.doi.org/10.1177/147323000203000317.

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The efficacy and safety profiles of barnidipine in the treatment of hypertension were evaluated in an open parallel-group study. Fifty-nine Chinese patients with mild-to-moderate essential hypertension were randomized to receive either barnidipine or felodipine (5 mg once daily, titrated to 10 mg or 15 mg once daily, as indicated) for 12 weeks. Both drugs reduced blood pressures significantly with ≥ 68% of cases obtaining marked or moderate blood pressure reduction. Mean reductions in systolic and diastolic blood pressure for barnidipine treatment were 23.7 ± 13.5 mmHg and 12.7 ± 7.9 mmHg, and for felodipine, 24.3 ± 18.4 mmHg and 14.5 ± 10.0 mmHg, respectively. There was no significant difference between these two drugs in anti-hypertensive effect, heart rate, laboratory measurements or incidence of adverse events. The only difference was that more patients taking felodipine experienced palpitations. We conclude that barnidipine has similar efficacy and a similar safety profile to felodipine in the treatment of mild-to-moderate essential hypertension in Chinese patients.

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36

Li, Shuxian, Jialuo Bu, Wenbin Liu, Cuijuan Liu, and Yuguang Lv. "Study on the fluorescence properties of the interaction between felodipine and bovine serum protein." E3S Web of Conferences 300 (2021): 01023. http://dx.doi.org/10.1051/e3sconf/202130001023.

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The interaction between felodipine and bovine serum protein was studied, the optimal experimental conditions were selected, and the fluorescence quenching mechanism was discussed. The interaction between filodipine and bovine serum protein was determined by UV spectrophotometry, and the optimal experimental conditions were selected by control variable method. The mechanism of fluorescence quenching in the system was explored by fluorescence spectrophotometry. The fluorescence intensity of the system between felodipine and bovine serum protein was the most obvious under the experimental conditions of buffer solution pH 7.4, felodipine concentration 8.0*10-4mol/L, reaction time 30min and 25°C. Static fluorescence quenching caused by the formation of complex compounds.

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37

Chretien, Marc L., David G. Bailey, Linda Asher, Jeremy Parfitt, David Driman, Jamie Gregor, and George K. Dresser. "Severity of coeliac disease and clinical management study when using a CYP3A4 metabolised medication: a phase I pharmacokinetic study." BMJ Open 10, no. 3 (March 2020): e034086. http://dx.doi.org/10.1136/bmjopen-2019-034086.

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ObjectiveSeverity of coeliac disease depends in part on the extent of small intestinal mucosa injury. Patients with the most abnormal pathology have loss of duodenal villi CYP3A4, a drug-metabolising enzyme that inactivates many drugs. These patients are hypothesised to have greater systemic concentrations of felodipine, a drug which normally has low oral bioavailability secondary to intestinal CYP3A4-mediated metabolism. It serves as a representative for a class containing many medications.DesignA phase I, open-label, single-dose, pharmacokinetic study.SettingLondon, Ontario, Canada.ParticipantsPatients with coeliac disease (n=47) with positive serology and healthy individuals (n=68).Main outcome measuresPatients with coeliac disease—upper gastrointestinal endoscopy and oral felodipine pharmacokinetics study within a 3-week period. Healthy individuals—oral felodipine pharmacokinetics study with water and grapefruit juice.ResultsCoeliac stratification categories: Group A (n=15, normal), B+C (n=16, intraepithelial lymphocytosis with/without mild villous blunting) and D (n=16, moderate/severe villous blunting). Groups A, B+C and D had linear trends of increasing felodipine AUC0–8; mean±SEM, 14.4±2.1, 17.6±2.8, 25.7±5.0; p<0.05) and Cmax (3.5±0.5, 4.0±0.6, 6.4±1.1; p<0.02), respectively. Healthy subjects receiving water had lower felodipine AUC0–8(11.9±0.9 vs 26.9±0.9, p=0.0001) and Cmax (2.9±0.2 vs 7.7±0.2, p=0.0001) relative to those receiving grapefruit juice.ConclusionsIncreased felodipine concentrations in patients with coeliac disease were most probably secondary to decreased small intestinal CYP3A4 expression. Patients with severe coeliac disease and healthy individuals with grapefruit juice had equivalently enhanced effect. Thus, patients with severe coeliac disease would probably experience similarly altered drug response, including overdose toxicity, from many important medications known to be metabolised by CYP3A4. Patients with coeliac disease with severe disease should be considered for other clinical drug management, particularly when there is the potential for serious drug toxicity.

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38

B. Hamed, Sumaya, and Shaimaa N. Abd Alhammid. "Formulation and Characterization of Felodipine as an Oral Nanoemulsions." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 30, no. 1 (June 15, 2021): 209–17. http://dx.doi.org/10.31351/vol30iss1pp209-217.

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Felodipine is a calcium-channel blocker with low aqueous solubility and bioavailability. Lipid dosage forms are attractive delivery systems for such hydrophobic drug molecules. Nanoemulsion (NE) is one of the popular methods that has been used to solve the dispersibility problems of many drugs. Felodipine was formulated as a NE utilizing oleic acid as an oil phase, tween 80 and tween 60 as surfactants and ethanol as a co-surfactant. Eight formulas were prepared, and different tests were performed to ensure the stability of the NEs, such as particle size, polydispersity index, zeta potential, dilution test, drug content, viscosity and in-vitro drug release. Results of characterization showed that felodipine nanoemulsion (F3) with (oleic acid 10%) ,(Smix 60% of tween80 :ethanol in a ratio of 3:1), (DDW 30%) was selected as the best formula, since it has a particle size of (17.01)nm, low PDI (0.392), zeta potential (-22.34mV), good dilution without drug precipitation , higher percent of drug content (99.098%) with acceptable viscosity , and complete release of the drug after (45 min.) with significantly higher (P<0.05) dissolution rate in comparison with the pure drug powder. The selected formula (F3) subjected to further investigations as drug and excipient compatibility study by Fourier transform infrared spectroscopy (FTIR) The outcomes of the (FTIR) explain that the distinctive peaks for felodipine were not affected by other components and displayed the same functional group's band with very slight shifting. This indicates that there was no interaction between felodipine and other NE components. Therefore, these excipients were found to be compatible with felodipine. In conclusion, the NE was found to be an efficient method to enhance the dispersibility and permeatioins of drugs that have poor water solubility (lipophilic drugs).

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Katzman, P. L., G. F. DiBona, B. Hökfelt, and U. L. Hulthén. "Acute renal tubular and hemodynamic effects of the calcium antagonist felodipine in healthy volunteers." Journal of the American Society of Nephrology 2, no. 5 (November 1991): 1000–1006. http://dx.doi.org/10.1681/asn.v251000.

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To evaluate the renal tubular effects of felodipine in a low (1.25-mg) and a high (10-mg) dose, lithium clearance was measured and related to renal hemodynamics in 10 healthy volunteers. After felodipine (1.25 mg), mean blood pressure decreased 4 mm Hg and heart rate increased 4 beats per minute. GFR and renal hemodynamics were unaltered. Natriuresis and diuresis increased and lithium clearance and fractional excretion of lithium were unchanged as compared with placebo. Felodipine (10 mg) decreased mean blood pressure 8 mm Hg; heart rate increased 16 beats per minute, and plasma catecholamines were elevated. GFR was unaltered, whereas RBF increased and renal vascular resistance decreased. Natriuresis and diuresis were further increased, and lithium clearance and fractional excretion of lithium were elevated. In conclusion, felodipine in a low dose of 1.25 mg, which did not change renal hemodynamics, had natriuretic and diuretic effects at a predominantly postproximal tubular site, whereas a high dose of 10 mg, which increased RBF and decreased renal vascular resistance, had additional natriuretic and diuretic effects in the proximal tubule.

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Vetchy, David, Martina Vetcha, Miloslava Rabiškova, Eva Gryczova, and Lenka Bartošikova. "Comparison in vitro felodipine release rate from the original versus generic product with controlled release of the drug." Medicina 43, no. 4 (April 4, 2007): 326. http://dx.doi.org/10.3390/medicina43040040.

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After patent protection of original brand is over, there are a lot of generic products occurring on the pharmaceutical market. It may be the way to reduce the price, but on the other hand, one should expect the same quality and almost identity with original brand, because the development of generic drugs is based on pharmacological properties of the original brand. The aim of this study was to compare the similarity of two products with controlled release of felodipine – generic product Presid® and original brand Plendil® – which are commercially available in Czech Republic, based on in vitro dissolution testing. The dissolution test in three dissolution media of increasing pH (1.2, 4.5, and 6.5) for the simulation of physiological pH within the gastrointestinal tract confirmed controlled release of felodipine from the original product Plendil ER 5 mg and Plendil ER 10 mg during the period of 24 hours. The release of felodipine from generic products Presid 5 mg and Presid 10 mg was not controlled for 24 hours as it is indicated in the information leaflet. In the generic products, felodipine release was controlled just for 12 or 18 hours and in this respect did not show similarity with the original brand. Since patients take the drug just once a day in the morning, the controlled release of felodipine, which lasts only 12 to 18 hours, can cause insufficient blood pressure control especially in the most critical morning hours and higher cardiovascular risk.

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Sutfin, T. A., T. Lind, M. Gabrielsson, and C. G. Reg»rdh. "Biliary secretion of felodipine metabolites in man after intravenous [14C]felodipine." European Journal of Clinical Pharmacology 38, no. 5 (May 1990): 421–24. http://dx.doi.org/10.1007/bf02336677.

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Yan, Fang, Ying Hu, Bin Di, Ping Lei He, and Guibin Sun. "Effects of Some Antihypertensive Drugs on the Metabolism and Pharmacokinetics of Indapamide in Rats." Journal of Pharmacy & Pharmaceutical Sciences 15, no. 2 (February 26, 2012): 208. http://dx.doi.org/10.18433/j3sk5v.

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Purpose. Indapamide, a non-thiazide antihypertensive diuretic agent, has been widely coadministered with other classes of antihypertensive agents to reach target systolic blood pressure. Indapamide is extensively metabolized by cytochromes P450. Interaction of indapamide and other antihypertensive drugs are unknown. We investigated the effects of other antihypertensive drugs on the metabolism and pharmacokinetics of indapamide in vitro and in vivo. Methods. Indapamide metabolism was studies in vitro using human liver microsomes pretreated with or without different concentrations of CYP-selective inhibitors and seven major antihypertensive drugs, felodipine, nifedipine, nitrendipine, telmisartan, irbesartan, valsartan and puerarin. Furthermore, the pharmacokinetics of indapamide was determined by HPLC-MS/MS to evaluate the effects of felodipine coadministered on the bioavailability of indapamide in rats in vivo. Results. The Km and Vmax of indapamide metabolism were 114.35 ± 3.47 μM and 23.13 ± 6.61 μmol/g/min. The metabolites of indapamide, hydroxyl-indapamide and dehydrogen-indapamide, were followed. CYP3A4 and CYP2C19 were involved in indapamide metabolism in human live microsomes. In addition, felodipine, nifedipine and nitrendipine significantly inhibited indapamide metabolism with the maximum inhibitory rates of 82.6%, 72% and 95%, respectively. Felodipine significantly elevated indapamide plasma concentration and prolonged its half-life. Conclusions. Combination therapy of indapamide and felodipine might lead to the alteration of indapamide metabolism and pharmacokinetics. The consequence of such an interaction that may include increased effectiveness and side effect needs to be tudeis in human. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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&NA;. "SADRAC reports on felodipine." Reactions Weekly &NA;, no. 304 (June 1990): 1. http://dx.doi.org/10.2165/00128415-199003040-00002.

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&NA;. "Felodipine - a safety profile." Reactions Weekly &NA;, no. 306 (June 1990): 2. http://dx.doi.org/10.2165/00128415-199003060-00003.

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&NA;. "Felodipine and grapefruit juice." Drugs & Therapy Perspectives 4, no. 5 (September 1994): 11–12. http://dx.doi.org/10.2165/00042310-199404050-00006.

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Ljung, Bengt. "Vascular Selectivity of Felodipine." Drugs 29, Supplement 2 (1985): 46–58. http://dx.doi.org/10.2165/00003495-198500292-00011.

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Been, M., P. W. Macfarlane, and W. S. Hillis. "Electrophysiological Effects of Felodipine." Drugs 29, Supplement 2 (1985): 76–80. http://dx.doi.org/10.2165/00003495-198500292-00014.

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&NA;. "Itraconazole increases felodipine concentrations." Reactions Weekly &NA;, no. 657 (June 1997): 5. http://dx.doi.org/10.2165/00128415-199706570-00008.

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&NA;. "Itraconazole increases felodipine concentrations ???" Inpharma Weekly &NA;, no. 1091 (June 1997): 20. http://dx.doi.org/10.2165/00128413-199710910-00041.

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Ljung, B., and M. Nordlander. "Pharmacodynamic Properties of Felodipine." Drugs 34, Supplement 3 (1987): 7–15. http://dx.doi.org/10.2165/00003495-198700343-00004.

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