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Carbamazepine, inhibition uptake

The anticonvulsants primidone and carbamazepine inhibit biotin uptake into brush-border membrane vesicles from human intestine (Zempleni et al. 2009). Long-term therapy with anticonvulsants increases both biotin catabolism and urinary excretion of 3-hydroxyisovaleric acid. These eifects might be due to displacement of biotin from biotinidase by anticonvulsants, thereby aifecting plasma transport, renal handling or cellular uptake of biotin. [Pg.185]

Mechanism of Action. These drugs are believed to exert their primary antiepileptic effects in a manner similar to phenytoin—that is, they stabilize the neuronal membrane by slowing the recovery of sodium channels firing too rapidly. Carbamazepine may also inhibit the presynaptic uptake and release of norepinephrine, and this effect may contribute to its antiseizure activity. [Pg.109]

Furthermore, we think that one may also conclude that the clinical effects of phenytoin, carbamazepine and lidocaine are most likely due to their inhibitory action on Na uptake rather than a primary action on Ca conductance. This is based on the finding that much lower concentrations of all three drugs are needed to inhibit veratridine-stimulated (i.e., Na-dependent) Ca uptake than are required to inhibit K-stiraulated (Na-independent) Ca uptake. This does not necessarily imply that an alteration of Ca conductances is not involved in the clinical effects of the above drugs. In the CNS, in situ, Ca uptake is stimulated by cellular depolarization which results from augmented Na influx. Obviously, impairment of Na influx by a drug would secondarily diminish Ca uptake. Also, at least in the case of phenytoin, direct inhibition of Ca uptake may have a role in its clinical effect. [Pg.155]


See other pages where Carbamazepine, inhibition uptake is mentioned: [Pg.556]    [Pg.499]    [Pg.33]    [Pg.31]    [Pg.306]    [Pg.147]    [Pg.153]    [Pg.154]    [Pg.154]    [Pg.17]   
See also in sourсe #XX -- [ Pg.148 , Pg.149 ]




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