Drugs online research references
J Pharmacol Exp Ther. 1985 Nov;235(2):313-8.
Furosemide choleresis in isolated perfused rat liver: partial dependency on perfusate sodium and chloride.
Anwer MS.
The effect of furosemide on hepatic bile formation was studied in isolated perfused rat liver to determine if 1) the observed cholestatic effect at lower dose of furosemide in vivo is a primary effect or a secondary effect due to decreased hepatic blood flow caused by the furosemide-induced volume contraction and if 2) the observed choleretic effect at higher doses can be explained by the osmotic effect of furosemide and its metabolites in bile. A single dose of furosemide (initial perfusate concentration 0.01, 0.1 or 1 mM) produced choleresis, whereas 0.001 mM furosemide did not affect bile flow significantly. Because furosemide failed to produce cholestasis at tested doses, the observed cholestasis in vivo at similar blood concentrations must be a secondary effect. Furosemide choleresis was associated with biliary secretion of furosemide and its metabolites. However, the choleretic effect expressed as microliters per micromole of drug secreted declined with increasing dose and biliary secretion. Furosemide choleresis was also associated with an increase in the net biliary secretion of Na+ and Cl-. The effect of Na+ and Cl- replacement on furosemide choleresis was studied to determine if the choleresis was a result of direct effect of furosemide on hepatic electrolyte transport. Replacement of perfusate Na+ completely by Li+ or partially by choline+ resulted in a 30 to 50% reduction in choleretic effect and furosemide-induced biliary Cl- secretion. A similar decline in choleretic effect and net furosemide-induced biliary Na+ secretion was also observed when perfusate Cl- was replaced by nitrate, acetate or isethionate.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2997429&dopt=Abstract
Comp Biochem Physiol Comp Physiol. 1994 Jun-Jul;108(2-3):297-302.
Ion transport across the isolated intestinal mucosa of Anguilla anguilla (Pisces).
Baldisserotto B, Mimura OM.
Departamento de Fisiologia, Universidade Federal de Santa Maria, RS, Brazil.
The posterior intestine of freshwater-adapted Anguilla anguilla has a serosa negative transepithelial potential difference (TPD), and a current corresponding to the flow of negative current towards serosa. The TPD and the short-circuit current (SCC) were inhibited by Na+ and K+ withdrawal, and Cl- substitution or BA2+ addition inverts TPD and SCC, suggesting a Cl- and Na+ current mucosa-serosa, a K(+)-Cl- cotransport and a K+ channel in the mucosal side. The TPD and SCC were inhibited by ouabain, DIDS, furosemide and amiloride, indicating the presence of a Na(+)-K(+)-ATPase, and Cl-/HCO3-,Na(+)-K(+)-Cl- and Na+/H+ cotransporters.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7520383&dopt=Abstract
Am J Physiol. 1989 Jan;256(1 Pt 1):G78-86.
Uptake of bumetanide into isolated rat hepatocytes and primary liver cell cultures.
Petzinger E, Muller N, Follmann W, Deutscher J, Kinne RK.
Max-Planck-Institut fur Systemphysiologie, Dortmund, Federal Republic of Germany.
Uptake of bumetanide into rat liver cells was investigated using isolated hepatocytes and primary cell cultures. The kinetics of [3H]-bumetanide uptake revealed two saturable components in addition to an unsaturable component. Saturable bumetanide uptake consists of a high-affinity, sodium-dependent uptake and a low-affinity transport system. Bumetanide uptake into isolated rat hepatocytes is energy dependent and temperature sensitive. At low temperatures, bumetanide uptake is due to diffusion with a permeability coefficient of 1.16 x 10(-6) cm/s. In primary liver cell cultures, uptake of bumetanide decreases rapidly over 3 days. AS-30D ascites hepatoma cells do not take up bumetanide but bind small amounts of the loop diuretic. Hepatocytes metabolized bumetanide extensively. The metabolites were secreted into the surrounding incubation buffer. Two hydroxylated and at least one conjugated biotransformation product could be separated by thin-layer chromatography. Isolated rat hepatocytes possess carrier proteins for uptake of bumetanide and very likely also for uptake of other loop diuretics like furosemide, piretanide, and torasemide. Several inhibitors of multispecific transport systems in the kidney and liver were tested as potential inhibitors of hepatocellular bumetanide or furosemide uptake. Probenecid, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, iodipamide, digitoxin, bile acids, and bromosulfophthalein inhibited uptake of loop diuretics. Inhibition by taurocholic acid was competitive with a Ki of 24 microM. Taurocholic acid inhibited [3H]bumetanide uptake in the presence but not in the absence of Na+. Deoxycholic acid and bromosulfophthalein were noncompetitive inhibitors of hepatocellular bumetanide uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2912153&dopt=Abstract
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