Influence of nisoldipine on haemodynamic effects and plasma levels of digoxin.

Kirch, Wilhelm; Stenzel, J.; Dylewicz, Piotr; Hutt, HJ; Santos, S. R.; Ohnhaus, E. E.

doi:10.1111/j.1365-2125.1986.tb05243.x

Cited by 23 publications

(7 citation statements)

References 15 publications

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“…The estimated IC50 value for simvastatin on [ 3 H]digoxin transport in LLC-GA5-COL150 cells was 48.2 l m , which was higher than those of the Ca 2 + blockers, nicardipine (4.54 l m ), manidipine (4.65 l m ) and benidipine (4.96 l m ), and comparable with that of nisoldipine (44.1 l m ) (unpublished results). The interaction of nisoldipine with digoxin was observed in clinical use, but the degree of the interaction was not signi® cant (Kirch et al 1986). The plasma concentration of simvastatin (40 mg}day) was around 50 l g equiv.…”

Section: [ 3 H]digoxin Transport At 3 H ( % Of Dose)mentioning

confidence: 99%

Simvastatin and lovastatin, but not pravastatin, interact with MDR1

Sakaeda

Takara

Kakumoto

et al. 2002

Journal of Pharmacy and Pharmacology

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The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, pravastatin, was compared with simvastatin and lovastatin from the viewpoint of susceptibility to interaction with or via the multidrug transporter, MDR1 (P-glycoprotein). This was carried out using the MDR1-overexpressing cell line LLC-GA5-COL150, established by transfection of MDR1 cDNA into porcine kidney epithelial LLC-PK1 cells, and [3H]digoxin, which is a well-documented substrate for MDR1. Pravastatin, at 25-100 microM, had no effect on the transcellular transport of [3H]digoxin whereas simvastatin and lovastatin suppressed the basal-to-apical transport of [3H]digoxin and increased the apical-to-basal transport. It was suggested that recognition by MDR1 was due to the hydrophobicity. In conclusion, simvastatin and lovastatin are susceptible to interaction with or via MDR1, but pravastatin is not. This is important information when selecting the HMG-CoA reductase inhibitors for patients taking drugs that are MDR1 substrates.

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Section: [ 3 H]digoxin Transport At 3 H ( % Of Dose)mentioning

confidence: 99%

Simvastatin and lovastatin, but not pravastatin, interact with MDR1

Sakaeda

Takara

Kakumoto

et al. 2002

Journal of Pharmacy and Pharmacology

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“…In a study by Kirch et al [79] trough plasma digoxin concentrations were elevated by about 15%. In a study by Kirch et al [79] trough plasma digoxin concentrations were elevated by about 15%.…”

Section: Nisoldipinementioning

confidence: 91%

“…[30] Coadministration of oral verapamil with oral atenolol [33] resulted in a variable increase in atenolol steady-state plasma concentrations in a group of patients receiving long term maintenance therapy with these 2 agents. These authors advocate limiting this combination to hospital practice because hospitalised patients can be more closely Kirch et al [79] Increase in digoxin concentration Continued over page McGourty et alf 34 ] noted improvement in the symptoms of angina pectoris in a high percentage of patients who were treated with both atenolol and verapamil, but a few patients developed congestive heart failure.…”

Section: 1 Afenololmentioning

confidence: 99%

Calcium Antagonists

Rosenthal

Ezra²

1995

Drug Safety

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The interaction of calcium antagonists, including the dihydropyridine calcium antagonists (e.g. nifedipine), verapamil and diltiazem, with drugs from other classes has major clinical ramifications as the use of drug combinations increases in frequency. Combinations are used in the treatment of disorders ranging from hypertension to cardiac rhythm disturbances, angina pectoris and peripheral vasospastic disease. In this era of organ transplantation, drugs like cyclosporin are coming into potential conflict with an ever-growing list of drugs. Drug combinations used as part of long term therapies are also making their appearance in toxic drug reactions, including antituberculous and anticonvulsant agents. Bronchodilators and H2-blockers also fall into this category of potential culprits of combined drug toxicity, and the interactions of calcium antagonists with beta-blockers and antiarrhythmic agents are also becoming a matter of concern.

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“…Nisoldipine increases blood digoxin levels by about 16% to 20% [102]. Nisoldipine increases bioavailability of propranolol, presumably by increasing splanchnic blood flow and decreasing the rate of first-pass metabolism of propranolol [103].…”

Section: Drug Interactionsmentioning

confidence: 99%

Calcium channel antagonists: part VI: Clinical pharmacokinetics of first and second-generation agents

Opie

1989

Cardiovasc Drug Ther

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A survey of the pharmacokinetic properties of the three prototypical calcium antagonist agents shows that they have in common a very high rate of hepatic first-pass metabolism with, in the case of verapamil and diltiazem, the formation of an active metabolite that affects the dose during chronic therapy. Therefore, the major factor altering the pharmacokinetic properties and the dose of the drug required is the capacity of the liver to metabolize the drug, which in turn depends on the hepatic blood flow and the activity of the hepatic metabolizing systems. Hence liver disease, a low cardiac output, and coadministration of certain drugs inducing or inhibiting the hepatic enzymes, all indirectly affect the pharmacokinetic properties of the calcium antagonists. There are also other potential drug interactions of a kinetic or dynamic nature that may arise. In general, renal disease has little effect on the pharmacokinetics of calcium antagonists.

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Influence of nisoldipine on haemodynamic effects and plasma levels of digoxin.

Cited by 23 publications

References 15 publications

Simvastatin and lovastatin, but not pravastatin, interact with MDR1

Simvastatin and lovastatin, but not pravastatin, interact with MDR1

Calcium Antagonists

Calcium channel antagonists: part VI: Clinical pharmacokinetics of first and second-generation agents

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