Drugs online research references
Drug Nutr Interact. 1981;1(1):45-53.
Inhibition of 5-methyltetrahydrofolic acid transport by amphipathic drugs.
Branda RF, Nelson NL.
Numerous chemically unrelated drugs after the membrane transport of folate compounds. To investigate drug structure-activity relationships, we measured the effect of amphipathic drugs (that is, compounds with polar-apolar character) on 5-methyltetrahydrofolic acid permeability of human erythrocytes. All drugs tested were inhibitory, but only compounds that exist at least partially in the anionic form were highly active. Ethacrynic acid, sulfinpyrazone, phenylbutazone, sulfasalazine, and furosemide were effective transport inhibitors in micromolar concentrations. In contrast, compounds that are capable of forming cations at physiologic pH, such as chlorpromazine, procaine, tetracaine, and papaverine, were inhibitory only in millimolar concentrations or caused hemolysis before major inhibition was seen. Inhibitory activity correlated with drug dissociation constant (r = 0.87). A double-reciprocal plot analysis of drug effect on 5-methyltetrahydrofolic acid transport showed changes in both Km and Vmax (indicating a mixture of competitive and noncompetitive inhibition) by ethacrynic acid, sulfasalazine, and phlorizin. Inhibitory activity of a series of eight phenoxyacetic derivatives, including ethacrynic acid, correlated highly with measurements of liposolubility (r = 0.87) but only weakly with the Hammet substituent constant (r = 0.56). These results suggest that the effect of amphipathic drugs on 5-methyltetrahydrofolic acid transport is influenced by drug pKa and by the presence of hydrophobic substituents, but is relatively independent of electron-attracting groups.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6926815&dopt=Abstract
Am J Physiol. 1995 Sep;269(3 Pt 2):R572-7.
Sulfate/oxalate exchange by lobster hepatopancreatic basolateral membrane vesicles.
Gerencser GA, Cattey MA, Ahearn GA.
Department of Physiology, College of Medicine, University of Florida, Gainesville 32610, USA.
Purified basolateral membrane vesicles (BLMV) were prepared from lobster hepatopancreas by osmotic disruption and discontinuous sucrose gradient centrifugation. Radiolabeled sulfate uptake was stimulated by 10 mM intravesicular oxalate compared with gluconate-loaded vesicles. Sulfate/oxalate exchange was not affected by transmembrane valinomycin-induced potassium diffusion potentials (inside negative or inside positive), suggesting electroneutral anion transport. Sulfate uptake was not stimulated by the similar carboxylic anions formate, succinate, oxaloacetate, or ketoglutarate. Sulfate influx occurred by at least one saturable Michaelis-Menten carrier system [apparent Km = 6.0 +/- 1.7 mM; maximum flux (Jmax) = 382.3 +/- 37.0 pmol.mg protein-1 x 7 s-1]. Sulfate/oxalate exchange was significantly reduced by the anion antiport inhibitors 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid but was not affected by bumetanide or furosemide. The possible physiological role of this exchange mechanism in anion/sulfate transport across the crustacean hepatopancreas is discussed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7573558&dopt=Abstract
J Appl Physiol. 1994 Jun;76(6):2651-5.
Acute respiratory acidosis: large-dose furosemide and cerebrospinal fluid ions.
Javaheri S, Corbett W, Adams JM, Davis PJ, Gartside PS.
Department of Veterans Affairs Medical Center, University of Cincinnati College of Medicine, Ohio 45220.
NaCl cotransport carrier is known to be involved in transepithelial fluid absorption and secretion in various tissues. Recent studies indicate that Na-K-2Cl cotransport carrier also exists in the choroid plexus cells and that inhibition of the carrier decreases cerebrospinal fluid (CSF) production. In this study, we used large-dose intravenous furosemide, an inhibitor of Na-K-2Cl carrier, to determine the effects on cisternal CSF ionic composition in acute respiratory acidosis. In pentobarbital-anesthetized mechanically ventilated dogs, renal pedicles were ligated to prevent furosemide-induced diuresis. The experimental group (group II, n = 7) received 400 mg/kg of furosemide intravenously, and group I (control group, n = 7) received the vehicle. In group II, serial serum and CSF furosemide concentrations were approximately 10(-3) and 10(-5) mol/l, respectively. During 5 h of acute respiratory acidosis in both groups, the mean arterial PCO2 increased approximately 25 Torr, with comparable changes in CSF PCO2. In both groups, CSF [HCO3-] and [H+] rose approximately 3 meq/l and 20 neq/l, respectively. Changes in CSF [Na+], [K+], [Cl-], and [Na(+)-Cl-] were also similar and were not significantly different from each other when the two groups were compared. These data show that furosemide at the dose that inhibits NaCl cotransport carrier does not significantly alter ionic composition of cisternal CSF.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7928896&dopt=Abstract
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