Drugs online research references
J Membr Biol. 1990 Jan;113(1):1-12.
Sulfhydryl-reactive heavy metals increase cell membrane K+ and Ca2+ transport in renal proximal tubule.
Kone BC, Brenner RM, Gullans SR.
Renal Division, Brigham and Women's Hospital, Boston, Massachusetts.
The cellular mechanisms by which nephrotoxic heavy metals injure the proximal tubule are incompletely defined. We used extracellular electrodes to measure the early effects of heavy metals and other sulfhydryl reagents on net K+ and Ca2+ transport and respiration (QO2) of proximal tubule suspensions. Hg2+, Cu2+, and Au3+ (10(-4)M) each caused a rapid net K+ efflux and a delayed inhibition of QO2. The Hg2(+)-induced net K+ release represented passive K+ transport and was not inhibited by barium, tetraethylammonium, or furosemide. Both Hg2+ and Ag+ promoted a net Ca2+ uptake that was nearly coincident with the onset of the net K+ efflux. A delayed inhibition of ouabain-sensitive QO2 and nystatin-stimulated QO2, indicative of Na+, K(+)-ATPase inhibition, was observed after 30 sec of exposure to Hg2+. More prolonged treatment (2 min) of the tubules with Hg2+ resulted in a 40% reduction in the CCCP-uncoupled QO2, indicating delayed injury to the mitochondria. The net K+ efflux was mimicked by the sulfhydryl reagents pCMBS and N-ethylmale-imide (10(-4) M) and prevented by dithiothreitol (DTT) or reduced glutathione (GSH) (10(-4) M). In addition, both DTT and GSH immediately reversed the Ag(+)-induced net Ca2+ uptake. Thus, sulfhydryl-reactive heavy metals cause rapid, dramatic changes in the membrane ionic permeability of the proximal tubule before disrupting Na+, K(+)-ATPase activity or mitochondrial function. These alterations appear to be the result of an interaction of the metal ions with sulfhydryl groups of cell membrane proteins responsible for the modulation of cation permeability.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2304068&dopt=Abstract
Int J Clin Pharmacol Ther Toxicol. 1984 Mar;22(3):134-9.
Plasma protein binding of metbufen, a new non-steroid anti-inflammatory drug, in humans.
Brunner F, Zini R, Tillement JP.
The binding of 14C-metbufen to human serum albumin and to plasma of cirrhotic patients was measured by equilibrium dialysis at 37 degrees C, pH = 7.4. Between 0.37-373 microM, binding of metbufen to human serum is linear and 99% complete. HSA is the only binding protein with two classes of saturable binding sites. The binding parameters are n1 = 3-5; K1 = 40000 M-1; n2 = 5-8; K2 = 2000 M-1 and n1 = 2; K1 = 148000 M-1, n2 = 7.5; K2 = 2800 M-1 to serum (600 microM HSA) and HSA (600 microM), respectively. The higher affinity constants of pure commercial HSA than found in serum and the lower number of binding sites are thought to be due to albumin polymerization in commercial HSA. In plasma from cirrhotic patients (total bilirubin: 232 microM; HSA = 450 microM), at 7.5 and 30 microM, metbufen-free fractions increased from 1.4 to 2.4% and 1.3 to 3.6%, respectively. At 2 or 8 micrograms/ml, metbufen is not displaced by salicylic acid (300 micrograms/ml), CPIB (200 micrograms/ml), furosemide (2 micrograms/ml), itanoxone (20 micrograms/ml), tolbutamide (100 micrograms/ml), warfarin (3 micrograms/ml), or diazepam (0.75 micrograms/ml). Finally, metbufen interacts with both the diazepam and warfarin binding sites of HSA to some degree.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6201451&dopt=Abstract
J Pharm Sci. 1976 OCT;65(10):1456-60.
Absorption, distribution, metabolism, and excretion of furosemide in dogs and monkeys I: analytical methodology, metabolism, and urinary excretion.
Yakatan GJ, Maness DD, Scholler J, Novick WJ Jr, Doluisio JT.
35S-Furosemide was administered to beagle dogs and rhesus monkeys in an oral solution on a single and a 20 repeated 5-mg/kg/day dosing regimen. Following the single dose, 25.0% (dogs) and 24.0% (monkeys) of the dose were excreted in the urine in 24 hr. TLC analysis demonstrated that both species had similar excretory patterns; i.e., over 80% of the amount excreted in the urine was present as unchanged durosemide and the remainder was composed of a known metabolite, saluamine, and an as yet unidentified metabolite(s). The repetitive dosing regimen did not appear to alter significantly either the total amount recovered in the 24-hr urine or the excretion pattern. Studies in dogs showed that only 50-60% of furosemide was absorbed from oral solution. A significant biliary secretion elimination pathway for furosemide also was observed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=824434&dopt=Abstract
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