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Propranolol metabolism

Masubuchi Y, Hosokawa S, Horie T, Suzuki T, Ohmori S, et al. 1994. Cytochrome P450 isozymes involved in propranolol metabolism in human liver microsomes. The role of CYP2D6 as ring-hydroxylase and CYP1A2 as N-desisopro-pylase. Drug Metab Dispos 22 909-915. [Pg.86]

Feely J, Wilkinson GR, Wood AJ. Reduction of liver blood flow and propranolol metabolism by cimetidine. N Engl J Med 1981 304(12) 692-5. [Pg.478]

Tateishi T, Ohashi K, Fujimura A, Ebihara A. The influence of diltiazem versus cimetidine on propranolol metabolism. J Chn Pharmacol 1992 32(12) 1099-104. [Pg.779]

Feely, J., Wilkinson, G.R. Wood, A.J.J. (1981) Reduction of liver blood flow and propranolol metabolism by cimetidine. New England Journal of Medicine, 304, 692-695. Finco, D.R., Brown, S.A., Vaden, S.L. Ferguson, D.C. (1995) Relationship between plasma creatinine concentration and glomerular filtration rate in dogs. Journal of... [Pg.131]

WL Nelson, TR Burke Jr. Pathways of propranolol metabolism use of the stable isotope twin-ion GC-MS technique to examine the conversion of propranolol to propranolol-diol by 9000g rat liver supernatant. Res Commun Chem Pathol Pharmacol 21 77-85,1978. [Pg.352]

Walle, T., Walle, U. K., Olanoff, L. S. Quantitative account of propranolol metabolism in urine of normal man. Drug Metab. Dispos. 1985,13, 204-209. [Pg.672]

Propranolol metabolism is affected by genetic polymorphism for both CYPIA (mephenytoin hydroxylation) and CYP2D6 (debrisoquine hydroxylation) isozymes in the liver [36,37]. Based on in vivo studies [36] in poor and extensive metabolizers of debrisoquine and mephenytoin and in vitro studies [37] using human liver microsomes and CYP isoforms, it appears that N-dealkylation of propranolol is mainly governed by S-mephenytoin-4-hydroxylase (CYPIA subfamily), whereas ring hydroxylation is predominantly related to debrisoquine isozyme (CYP2D6). [Pg.297]

Reilly CS, Biollaz J, Koshalgi RP, Wood AJJ. Enprostil, in contrast to cimetidine, does not inhibit propranolol metabolism. Clin Pharmacol Ther (1986) 40, 37-41. [Pg.846]

Vestal RE, Kcmhauser DM, HoUifield JW, Shand DG Inhibitic i of propranolol metabolism by chloipFomazine. CUnPharmacol Ther( 919) 25,19-24. [Pg.851]

Herman RJ, Nakamura K, Wilkinson GR, Wood AJJ. Induction of propranolol metabolism by rifampicin. BrJ Clin Pharmacol (1983) 16, 565-9. [Pg.855]

ShaheenO, Biollaz J, KoshakjiRP, Wilkinson GI Wood AJJ. Influence of debrisoquin phenotype on the inducibility of propranolol metabolism. Clin Pharmacol The r 9Z9) 45, 439-43. [Pg.855]

As propranolol is metabolised by CYP2D6 the US manufacturers suggest that inhibitors of this isoenzyme may inhibit propranolol metabolism. Some CYP2D6 inhibitors have been seen to interaet (such as quinidine , (p.853)), but the pharmacokinetic effects seem modest in many cases, probably because propranolol is also metabolised by CYP1A2. An interaction with ritonavir (as predicted by the manufacturers) therefore seems possible, and the effects may be greater than those seen with other CYP2D6 inhibitors (see (b) below). [Pg.858]

Because p-blockers decrease blood pressure and heart rate, they should be started at low doses to increase tolerability. Propranolol is hepatically metabolized, and its half-life and pharmacologic effects are prolonged in portal hypertension. A reasonable starting dose of propranolol is 10 mg two to three times daily. [Pg.332]

JW Paterson, ME Conolly, CT Dollery, A Hayes, RG Cooper. The pharmacodynamics and metabolism of propranolol in man. Pharmacol Clin 2 127-133, 1970. [Pg.422]

The answer is b. (Hardmanr p 906.) Cimetidine reversibly inhibits cytochrome P450. This is important in phase I bio transformation reactions and inhibits the metabolism of such drugs as warfarin, phenytoin, propranolol, metoprolol, quinidine, and theophylline. None of the other enzymes are significantly affected. [Pg.232]

There are pharmacokinetic differences among /1-blockers in first-pass metabolism, serum half-lives, degree of lipophilicity, and route of elimination. Propranolol and metoprolol undergo extensive first-pass metabolism. Atenolol and nadolol have relatively long half-lives and are excreted renally the dosage may need to be reduced in patients with moderate to severe renal insufficiency. Even though the half-lives of the other /J-blockers are much shorter, once-daily administration still may be effective. /J-Blockers vary in their lipophilic properties and thus CNS penetration. [Pg.134]

Blockers have been used widely to ameliorate thyrotoxic symptoms such as palpitations, anxiety, tremor, and heat intolerance. They have no effect on peripheral thyrotoxicosis and protein metabolism and do not reduce TSAb or prevent thyroid storm. Propranolol and nadolol partially block the conversion of T4 to T3, but this contribution to the overall therapeutic effect is small. [Pg.245]

The H2RAs are generally well tolerated. The most common adverse effects are headache, somnolence, fatigue, dizziness, and either constipation or diarrhea. Cimetidine may inhibit the metabolism of theophylline, warfarin, phenytoin, nifedipine, and propranolol, among other drugs. [Pg.282]

Rifampin Azoles, cyclosporine, methadone propranolol, Pis, oral contraceptives, tacrolimus, warfarin Increased metabolism of other agent Avoid if possible... [Pg.396]

Figure 6.19. Products of phosphatidylcholine metabolism. Phosphatidylcholine is metabolised to phosphatidic acid via the activity of phospholipase D. The phosphatidic acid generated in this way may then be converted into diacylglycerol via phosphatidate phospho-hydrolase (which is inhibited by propranolol), and the enzyme diacylglycerol kinase may regenerate the phosphatidic acid. Phospholipase D may also catalyse the transphosphati-dylation of primary alcohols, such as ethanol and butanol, at the expense of the natural substrate, phosphatidylcholine. Thus, primary alcohols can prevent phosphatidic acid production via this route. Figure 6.19. Products of phosphatidylcholine metabolism. Phosphatidylcholine is metabolised to phosphatidic acid via the activity of phospholipase D. The phosphatidic acid generated in this way may then be converted into diacylglycerol via phosphatidate phospho-hydrolase (which is inhibited by propranolol), and the enzyme diacylglycerol kinase may regenerate the phosphatidic acid. Phospholipase D may also catalyse the transphosphati-dylation of primary alcohols, such as ethanol and butanol, at the expense of the natural substrate, phosphatidylcholine. Thus, primary alcohols can prevent phosphatidic acid production via this route.
The c//-propranolol antiserum exhibits an almost equal affinity for both d- and /-isomers whilst the /-propranolol shows exclusively a marked and pronounced affinity for the /-isomer, By the application of these two RIA-techniques, it was practically feasible to quantify the plasma and heart concentrations of dl- and /-propranolol individually. Thus, the concentrations of d-propranolol could be arrived at by subtracting the concentration of /-isomer from the dl-mixture. It has been clearly demonstrated by Kawashima and coworkwers that the <7-propranolol undergoes distribution in vivo very sluggishly besides being metabolized more rapidly whereas the /-isomer gets distributed rather quickly to various tissues including the heart. [Pg.504]

B. D. Anderson, W. W. Chu, R. E. Galinsky, Reduction of First-Pass Metabolism of Propranolol after Oral Administration of Ester Prodrugs , Int. J. Pharm. 1988, 43,261 -265. [Pg.543]

Patients with hyperthyroidism tend to have enhanced metabolism leading to weight loss, tremor and palpitations. Propranolol may be indicated to reduce the sympathetic symptoms, such as tremor and palpitations. [Pg.252]

All these compounds are moderately lipophilic and should show excellent ability to cross biological membranes by transcellular absorption. Propranolol, betaxolol and metoprolol all have minimal gut first-pass metabolism, as shown by the low value for E(g. i.). Metabolism and first pass effects for these compounds are largely confirmed to the liver as shown by the values for E(g. i.). In contrast talinolol shows high extraction by the gastrointestinal tract with low liver extraction [13]. These effects are illustrated graphically in Figure 3.9 which shows the bioavailability predicted from hepatic extraction contrasted with that seen in vivo in man. [Pg.43]


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