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Edgar Selvaag - One of the best experts on this subject based on the ideXlab platform.
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Cell cultures in the investigation of thiazide phototoxicity.
Naunyn-schmiedebergs Archives of Pharmacology, 1997Co-Authors: Edgar SelvaagAbstract:The NHIK 3025 cell line (Norsk Hydro Institutt for Kreftforskning), a human in situ carcinoma of the cervix cell line, was used to investigate the thiazides bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, butizide, chlortalidone, furosemide, hydrochlorothiazide, hydroflumethiazide, indapamide, Piretanide, polythiazide, trichlormethiazide and xipamide for their potential phototoxic properties. Cell death following UVA irradiation and dependent on test substance concentration was observed in the presence of all the tested substances except chlortalidone, furosemide, indapamide and xipamide. Bendroflumethiazide was phototoxic at concentrations of 0.05mM and higher; bemetizide, benzylhydrochlorothiazide, bumetanide and hydroflumethiazide were phototoxic at 0.25mM and higher and butizide, hydrochlorothiazide, Piretanide, polythiazide and trichlormethiazide were phototoxic at 0.5mM and higher.
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In Vitro Phototoxicity Due to Sulfonamide-Derived Oral Antidiabetic and Diuretic Drugs
Journal of Toxicology-cutaneous and Ocular Toxicology, 1997Co-Authors: Edgar SelvaagAbstract:AbstractThe sulfonamide-derived oral antidiabetic agents chlorpropamide, glibenclamide, glipizide, gliquidone, glymidine, tolazamide, and tolbutamide, and the diuretics bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, tubizide, chlortalidone, furosemide, hydrochlorothiazide, hydroflumethiazide, indapamide, Piretanide, polythiazide, trichlormethiazide, and xipamide were investigated for phototoxicity in a cell culture model. Cell death dependent on ultraviolet A (UVA) fluence and test substance concentration was observed in the presence of the oral antidiabetics glibenclamide and gliquidone, as well as the diuretics bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, butizide, hydrochlorothiazide, hydroflumethiazide, Piretanide, polythiazide, and trichlormethiazide. Bendroflumethiazide was phototoxic at concentrations of 5 × 10−5 M and higher; bemetizide, benzylhydrochlorothiazide, bumetanide, and hydroflumethiazide were phototoxic at concentrations of 2.5 × 10−4 ...
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Inhibiting effects of antioxidants on drug-induced phototoxicity in cell cultures Investigations with sulphonamide-derived oral antidiabetics and diuretics
Journal of Photochemistry and Photobiology B-biology, 1997Co-Authors: Edgar Selvaag, Johan Emelian Moan, Helle Anholt, Per ThuneAbstract:The sulphonamide-derived oral antidiabetics chlorpropamide, glibenclamide, glipizide, gliquidone, glymidine, tolazamide and tolbutamide, and the diuretics bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, butizide, chlortalidone, furosemide, hydrochlorothiazide, hydroflumethiazide, indapamide, Piretanide, polythiazide, trichlormethiazide and xipamide were investigated for phototoxicity in a cell culture model. Cell death dependent on ultraviolet A (UVA) radiation fluence and test substance concentration was observed in the presence of the oral antidiabetics glibenclamide and gliquidone, as well as the diuretics bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, butizide, hydrochlorothiazide, hydroflumethiazide, Piretanide, polythiazide and trichlormethiazide. Bendroflumethiazide was phototoxic at concentrations of 0.05 mM and above; bemetizide, benzylhydrochlorothiazide, bumetanide and hydroflumethiazide were phototoxic at concentrations of 0.25 mM or more; the oral antidiabetics glibenclamide and gliquidone, as well as the diuretics butizide, hydrochlorothiazide, Piretanide, polythiazide and trichlormethiazide were phototoxic at concentrations of 0.5 mM. To evaluate the effects of antioxidants, ascorbic acid, alpha-tocopherol, beta-carotene or ubiquinone was added to the tissue culture flasks before irradiation. The phototoxic inhibition of the colony-forming ability was largely reduced by the addition of ascorbic acid and alpha-tocopherole, indicating the involvement of reactive oxygen species in the phototoxic process.
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Phototoxicity due to sulphonamide derived oral antidiabetics and diuretics: investigations in a cell culture model
Photodermatology Photoimmunology and Photomedicine, 1996Co-Authors: Edgar Selvaag, Johan Emelian Moan, Helle Anholt, Per ThuneAbstract:A number of sulphonamide-derived oral antidiabetics (chlorpropamide, glibenclamide, glipizide, gliquidone, glymidine, tolazamide and tolbutamide) and diuretics (bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, butizide, chlortalidone, furosemide, hydrochlorothiazide, hydroflumethiazide, indapamide, Piretanide, polythiazide, trichlormethiazide and xipamide) were investigated for phototoxicity in a cell culture model. Cell death dependent on ultraviolet A fluence and test substance concentration was observed in the presence of the oral antidiabetics glibenclamide and gliquidone, as well as the diuretics bemetizide, bendroflumethiazide, benzyl-hydrochlorothiazide, bumetanide, butizide, hydrochlorothiazide, hydroflumethiazide, Piretanide, polythiazide and trichlormethiazide. Bendroflumethiazide was phototoxic at 5times10−5 M and higher concentrations, bemetizide, benzylhydrochlorothiazide, bumetanide and hydroflumethiazide were phototoxic at 2.5times10−4 M and higher concentrations, and the oral antidiabetics glibenclamide and gliquidone as well as the diuretics butizide, hydrochlorothiazide, Piretanide, polythiazide and trichlormethiazide were phototoxic at 5−4 M and higher concentrations. Electron microscopic investigations showed swelling of mitochondria and endoplasmic reticulum as well as aggregation of euchromatin when the cells were irradiated in the presence of photosensitizers***
E. Mutschler - One of the best experts on this subject based on the ideXlab platform.
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Constant K^+/Na^+ excretion ratio during peak diuresis after Piretanide but insignificant K^+ loss during 24 hours
European Journal of Clinical Pharmacology, 1992Co-Authors: H. Knauf, E. MutschlerAbstract:The effect of Piretanide on Na^+ and K^+ excretion and on renal haemodynamics has been studied in 14 subjects with a GFR (Inulin clearance) ranging from 140 to 2 ml · min^−1. After a two day fluid and salt balance control period, oral Piretanide 6 mg induced a natriuresis and kaliuresis, which was proportional to the GFR of the patients. The ratio of drug-induced K^+ to Na^+ excretion was always 0.13, independent of individual GFR. This was only true for the duration of the action of Piretanide, τ , which was 6 h in subjects with normal GFR and 5 h in patients with impaired kidney function. Surprisingly, after τ , i. e. for 24 h after drug administration, less potassium was lost than in the pretreatment period. Neither the GFR nor the renal blood flow (PAH clearance) of the patients were affected by Piretanide. In conclusion, Piretanide given once a day was an effective natriuresic agent, even in end-stage renal disease, and it produced relatively little K^+-loss when given once daily.
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constant k na excretion ratio during peak diuresis after Piretanide but insignificant k loss during 24 hours
European Journal of Clinical Pharmacology, 1992Co-Authors: H. Knauf, E. MutschlerAbstract:The effect of Piretanide on Na+ and K+ excretion and on renal haemodynamics has been studied in 14 subjects with a GFR (Inulin clearance) ranging from 140 to 2 ml.min-1. After a two day fluid and salt balance control period, oral Piretanide 6 mg induced a natriuresis and kaliuresis, which was proportional to the GFR of the patients. The ratio of drug-induced K+ to Na+ excretion was always 0.13, independent of individual GFR. This was only true for the duration of the action of Piretanide, tau, which was 6 h in subjects with normal GFR and 5 h in patients with impaired kidney function. Surprisingly, after tau, i.e. for 24 h after drug administration, less potassium was lost than in the pretreatment period. Neither the GFR nor the renal blood flow (PAH clearance) of the patients were affected by Piretanide. In conclusion, Piretanide given once a day was an effective natriuretic agent, even in end-stage renal disease, and it produced relatively little K(+)-loss when given once daily.
Per Thune - One of the best experts on this subject based on the ideXlab platform.
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Inhibiting effects of antioxidants on drug-induced phototoxicity in cell cultures Investigations with sulphonamide-derived oral antidiabetics and diuretics
Journal of Photochemistry and Photobiology B-biology, 1997Co-Authors: Edgar Selvaag, Johan Emelian Moan, Helle Anholt, Per ThuneAbstract:The sulphonamide-derived oral antidiabetics chlorpropamide, glibenclamide, glipizide, gliquidone, glymidine, tolazamide and tolbutamide, and the diuretics bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, butizide, chlortalidone, furosemide, hydrochlorothiazide, hydroflumethiazide, indapamide, Piretanide, polythiazide, trichlormethiazide and xipamide were investigated for phototoxicity in a cell culture model. Cell death dependent on ultraviolet A (UVA) radiation fluence and test substance concentration was observed in the presence of the oral antidiabetics glibenclamide and gliquidone, as well as the diuretics bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, butizide, hydrochlorothiazide, hydroflumethiazide, Piretanide, polythiazide and trichlormethiazide. Bendroflumethiazide was phototoxic at concentrations of 0.05 mM and above; bemetizide, benzylhydrochlorothiazide, bumetanide and hydroflumethiazide were phototoxic at concentrations of 0.25 mM or more; the oral antidiabetics glibenclamide and gliquidone, as well as the diuretics butizide, hydrochlorothiazide, Piretanide, polythiazide and trichlormethiazide were phototoxic at concentrations of 0.5 mM. To evaluate the effects of antioxidants, ascorbic acid, alpha-tocopherol, beta-carotene or ubiquinone was added to the tissue culture flasks before irradiation. The phototoxic inhibition of the colony-forming ability was largely reduced by the addition of ascorbic acid and alpha-tocopherole, indicating the involvement of reactive oxygen species in the phototoxic process.
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Phototoxicity due to sulphonamide derived oral antidiabetics and diuretics: investigations in a cell culture model
Photodermatology Photoimmunology and Photomedicine, 1996Co-Authors: Edgar Selvaag, Johan Emelian Moan, Helle Anholt, Per ThuneAbstract:A number of sulphonamide-derived oral antidiabetics (chlorpropamide, glibenclamide, glipizide, gliquidone, glymidine, tolazamide and tolbutamide) and diuretics (bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, butizide, chlortalidone, furosemide, hydrochlorothiazide, hydroflumethiazide, indapamide, Piretanide, polythiazide, trichlormethiazide and xipamide) were investigated for phototoxicity in a cell culture model. Cell death dependent on ultraviolet A fluence and test substance concentration was observed in the presence of the oral antidiabetics glibenclamide and gliquidone, as well as the diuretics bemetizide, bendroflumethiazide, benzyl-hydrochlorothiazide, bumetanide, butizide, hydrochlorothiazide, hydroflumethiazide, Piretanide, polythiazide and trichlormethiazide. Bendroflumethiazide was phototoxic at 5times10−5 M and higher concentrations, bemetizide, benzylhydrochlorothiazide, bumetanide and hydroflumethiazide were phototoxic at 2.5times10−4 M and higher concentrations, and the oral antidiabetics glibenclamide and gliquidone as well as the diuretics butizide, hydrochlorothiazide, Piretanide, polythiazide and trichlormethiazide were phototoxic at 5−4 M and higher concentrations. Electron microscopic investigations showed swelling of mitochondria and endoplasmic reticulum as well as aggregation of euchromatin when the cells were irradiated in the presence of photosensitizers***
Vinzenz Hombach - One of the best experts on this subject based on the ideXlab platform.
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acute and chronic effects of a diuretic monotherapy with Piretanide in congestive heart failure a placebo controlled trial
Cardiovascular Drugs and Therapy, 1990Co-Authors: W Haerer, U Bauer, N Sultan, K Cernoch, N Mouselimis, K J Fehske, M Hetzel, M Stauch, Vinzenz HombachAbstract:To evaluate the acute and chronic effects of diuretic monotherapy with 3 mg Piretanide bid, 46 patients (pts) with congestive heart failure (NYHA II-III) secondary to coronary artery disease were studied. Within 3 weeks of therapy, the patients lost 1.6 kg body weight. Forty-four patients reported a subjective feeling of improvement. Echocardiographically, a highly significant (p<0.001) reduction of diastolic and systolic diameters was found, as well as an increase of fraction shortening. Chest x-ray indicated a reduction of heart volume from 1012±263 ml to 936±233 ml (p<0.001). The serum potassium level remained unchanged. A subgroup of 26 pts underwent invasive hemodynamic examinations. IV injection of 6 mg Piretanide resulted in an acute reduction of pulmonary wedge pressure (pc) from 20.2±5.3 mmHg to 11.9±5.0 mmHg (p<0.001); simultaneously a slight decrease of cardiac index from 3.2±0.6 l/min/m2 to 3.0±0.4 l/min/m2 was observed. Invasive control after 3 weeks of oral therapy showed no decline of the Piretanide effect. The exercise tolerance increased clearly from 135±161 Wmin to 249±268 Wmin (p<0.05). A control group of further 14 pts was treated with placebo only and did not show any significant changes of pc (20.0±6.4 mmHg vs. 22.8±19.2 mmHg), exercise tolerance, or other clinical parameters. Thus, the diuretic monotherapy of congestive heart failure with Piretanide is highly effective and shows a significant improvement in all clinical and hemodynamic parameters in the absence of any remarkable side effects.
Alain Doucet - One of the best experts on this subject based on the ideXlab platform.
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Differential Regulation of Collecting Duct Na+,K+-ATPase and K+ Excretion by Furosemide and Piretanide: Role of Bradykinin
Journal of the American Society of Nephrology, 2004Co-Authors: Bénédicte Buffin-meyer, Mauricio Younes-ibrahim, Ghazi El Mernissi, Lydie Cheval, Sophie Marsy, Michèle Grima, Jean-pierre Girolami, Alain DoucetAbstract:In response to chronic treatment with furosemide, collecting ducts adapt their function to the initial loss of Na+ to prevent further Na+ loss and extracellular volume decrease. This adaptation, which includes the overexpression of Na+, K+-ATPase, is thought to account for most of the kaliuretic effect of furosemide. Because Piretanide is reported to be less kaliuretic than equidiuretic doses of furosemide, the authors compared the effects of 1-wk treatment with the two loop diuretics on urinary potassium excretion and on Na+, K+-ATPase activity in the collecting duct. At equidiuretic and equinatriuretic doses, furosemide increased urinary potassium excretion as well as collecting duct Na+, K+-ATPase activity, whereas Piretanide had no effect on either parameter. These effects of furosemide were curtailed by concomitant administration of the angiotensin-converting enzyme inhibitor enalapril, but they were not altered either by clamping changes in plasma aldosterone or by blocking type I angiotensin receptors. Treatment with the antagonist of bradykinin B2 receptors Hoe140 mimicked the two effects of furosemide. In addition, the effects of Hoe140 and furosemide were not additive. Finally, Piretanide increased urinary bradykinin excretion, whereas furosemide did not. These results suggest that induction of collecting duct Na+, K+-ATPase (a) accounts for the kaliuretic effect of furosemide, (b) is independent of the renin/angiotensin/aldosterone system, (c) results from increased Na+ delivery to the collecting duct and enhanced intracellular Na+ concentration, and (d) is prevented in Piretanide treated rats by increased bradykinin production that may limit apical Na+ entry in collecting duct principal cells.
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differential regulation of collecting duct na k atpase and k excretion by furosemide and Piretanide role of bradykinin
Journal of The American Society of Nephrology, 2004Co-Authors: Benedicte Buffinmeyer, Ghazi El Mernissi, Lydie Cheval, Sophie Marsy, Michèle Grima, Jean-pierre Girolami, Mauricio Younesibrahim, Alain DoucetAbstract:In response to chronic treatment with furosemide, collecting ducts adapt their function to the initial loss of Na+ to prevent further Na+ loss and extracellular volume decrease. This adaptation, which includes the overexpression of Na+, K+-ATPase, is thought to account for most of the kaliuretic effect of furosemide. Because Piretanide is reported to be less kaliuretic than equidiuretic doses of furosemide, the authors compared the effects of 1-wk treatment with the two loop diuretics on urinary potassium excretion and on Na+, K+-ATPase activity in the collecting duct. At equidiuretic and equinatriuretic doses, furosemide increased urinary potassium excretion as well as collecting duct Na+, K+-ATPase activity, whereas Piretanide had no effect on either parameter. These effects of furosemide were curtailed by concomitant administration of the angiotensin-converting enzyme inhibitor enalapril, but they were not altered either by clamping changes in plasma aldosterone or by blocking type I angiotensin receptors. Treatment with the antagonist of bradykinin B2 receptors Hoe140 mimicked the two effects of furosemide. In addition, the effects of Hoe140 and furosemide were not additive. Finally, Piretanide increased urinary bradykinin excretion, whereas furosemide did not. These results suggest that induction of collecting duct Na+, K+-ATPase (a) accounts for the kaliuretic effect of furosemide, (b) is independent of the renin/angiotensin/aldosterone system, (c) results from increased Na+ delivery to the collecting duct and enhanced intracellular Na+ concentration, and (d) is prevented in Piretanide treated rats by increased bradykinin production that may limit apical Na+ entry in collecting duct principal cells.