• Corpus ID: 46228651

The genetic control of bufuralol metabolism in man.

@article{Dayer1982TheGC,
  title={The genetic control of bufuralol metabolism in man.},
  author={Pierre Dayer and Luc P. Balant and F. Courvoisier and A. Kupfer and A. Kubli and A. Gorgia and Jean Fabre},
  journal={European journal of drug metabolism and pharmacokinetics},
  year={1982},
  volume={7 1},
  pages={
          73-7
        }
}
  • P. Dayer, L. Balant, J. Fabre
  • Published 1982
  • Medicine, Biology, Chemistry
  • European journal of drug metabolism and pharmacokinetics
Bufuralol (Ro 3 - 4787, Angium) is a non selective beta-adrenoceptor blocking drug with some degree of sympathomimetic action and a longer duration of action than propranolol. Plasma concentrations of bufuralol and 1'-hydroxybufuralol, its main blood derivative which shows similar beta-adrenoceptor blocking properties, were determined in healthy volunteers after a 60 mg oral and a 20 mg intravenous dose. Peak plasma concentrations were higher for the parent drug but due to a longer elimination… 
Relationship between pharmacokinetic and pharmacodynamic behaviour of bufuralol and its metabolite Ro 3-7410 in hypertensive patients
SummaryThe relationship between the plasma concentrations of bufuralol and its major hydroxymetabolite (Ro 3-7410) and β-blocking activity was studied in 10 patients with uncomplicated essential
Oxidation phenotype and the metabolism and action of beta-blockers
  • M. Lennard
  • Biology, Medicine
    Klinische Wochenschrift
  • 2005
TLDR
Variability in response to some drugs such as debrisoquine can be attributed to genetic polymorphism of their oxidative metabolism, which is a major determinant of the metabolism, pharmacokinetics and some of the pharmacological actions of metoprolol, bufuralol and timolol.
Stereo- and regioselectivity of hepatic oxidation in man — Effect of the debrisoquine/sparteine phenotype on bufuralol hydroxylation
TLDR
In vivo observations are in agreement with recent in vitro data obtained in human liver microsomes from phenotyped patients and support the concept of deficiency of a highly stereoselective cytochrome P-450 isozyme as the cause of this polymorphism.
Bufuralol metabolism in human liver: a sensitive probe for the debrisoquine‐type polymorphism of drug oxidation
TLDR
Microsomes of one individual identified as poor metabolizer of debrisoquine in vivo showed reduction of carbinol formation to 1·97 nmol mg‐ h‐1, and Mixing his microsomes with those of an extensive metabolizer resulted in additive formation ofcarbinol excluding mediation of the defect by a soluble inhibitor.
Importance of oxidative polymorphism and levomepromazine treatment on the steady-state blood concentrations of clomipramine and its major metabolites
TLDR
The results suggest that benzodiazepines rather than levomepromazine should be used in depressed patients with anxiety and/or agitation in combination with the antidepressant treatment.
Interactions of bupranolol with the polymorphic debrisoquine/sparteine monooxygenase (CYP2D6)
TLDR
Although the methods were not sufficiently sensitive to measure the Km of bupranolol directly, it is undoubtedly the β-adrenoceptor blocker with the highest-known apparent affinity for CYP2D6.
Effect of oxidative polymorphism (debrisoquine/sparteine type) on hepatic first-pass metabolism of bufuralol
TLDR
Bufuralol is a beta-adrenoceptor blocking drug whose oxidative metabolism is under the same genetic control as debrisoquine and sparteine and non-linear kinetics may occur after oral administration of bufuralol.
Contribution of the genetic status of oxidative metabolism to variability in the plasma concentrations of beta-adrenoceptor blocking agents
TLDR
The oxidative metabolism of bufuralol is under the same genetic control as that of debrisoquine and sparteine and the genetic oxidative status is a major source of interindividual variation in the plasma concentration of drugs that undergo oxidative metabolism.
Polymorphic hydroxylation of perhexiline maleate in man.
TLDR
Pretreatment phenotyping using this test, followed by exclusion of poor metabolisers from perhexiline therapy, should substantially reduce the incidence of major adverse effects.
Similar effect of oxidation deficiency (debrisoquine polymorphism) and quinidine on the apparent volume of distribution of (±)-metoprolol
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Despite the small number of subjects, (±)-metoprolol distribution appeared to be different both in genetically and environmentally (quinidine)-determined poor metabolisers, and quinidine inhibition was a good, reversible in vivo model of the genetic deficiency in handling (±-metoprool).
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