Drugs online research references
Proc Soc Exp Biol Med. 1989 Dec;192(3):276-80.
Urate excretion by the isolated perfused rat kidney and modification by drugs.
MacDougall ML, Wiegmann TB.
Department of Medicine, University of Kansas Medical Center, Kansas City 66103.
Urate excretion in the isolated perfused rat kidney was studied over a wide range of perfusate urate concentrations (13.9-376.8 microM). Fractional excretion of urate (FEurate) averaged 57.9 +/- 2.0% (range, 58.5-59.6%), showed marked interanimal variability, but was not dependent on the perfusate-free urate concentration. In paired experiments, the effects of five drugs (probenecid, pyrazinoate, furosemide, salicylate, and oxonate) on FEurate were evaluated. A low concentration of pyrazinoate (0.2 mM) decreased FEurate (62.0 +/- 1.9 vs 53.8 +/- 2.4%, P less than 0.05), as did 0.8 mM pyrazinoate (59.5 +/- 2.4 vs 48.4 +/- 2.7%, P less than 0.05). Probenecid (1 mM) decreased FEurate (59.3 +/- 3.1 vs 52.0 +/- 2.5%, P less than 0.05) but 2.5 mM probenecid did not alter FEurate (48.0 +/- 6.3 vs 47.8 +/- 6.9%). Oxonate (0.1 mM) also decreased FEurate (75.8 +/- 4.2 vs 67.1 +/- 2.1%, P less than 0.05) while 0.2 mM oxonate had no effect (66.4 +/- 3.5 vs 61.5 +/- 4.6%). Neither salicylate nor furosemide affected FEurate, although both drugs caused a saliuresis and diuresis. Thus, urate transport in rat kidneys in vitro is not dependent on urate concentration, unlike man. Some drugs known to affect urate excretion in humans and rats did not have similar effects in isolated kidneys. Isolated organ studies provide additional information is understanding renal urate handling.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2602393&dopt=Abstract
Toxicology. 1987 Feb;43(2):149-60.
Furosemide toxicity in isolated mouse hepatocyte suspensions.
Massey TE, Walker RM, McElligott TF, Racz WJ.
Incubation of freshly isolated mouse hepatocytes with 0.5 or 1.0 mM furosemide caused a depletion of cellular acid soluble sulfhydryls to approximately 20-30% of control over the course of 4.5 h. The depletion was accompanied by a reduction in cell viability (indicated by the lactate dehydrogenase latency test) which was significant (P less than 0.05) for 0.5 mM but not for 1.0 mM furosemide at 4.5 h. Ultrastructurally, 0.5 or 1.0 mM furosemide caused cytoplasmic changes including loss of glycogen, disaggregation of polyribosomes, vesiculation of endoplasmic reticulum, and occasional appearance of lamellar bodies consisting of concentric arrays of paired smooth membranes. These concentrations of furosemide also caused cell surface changes, including loss of microvilli, development of an irregular shape compared to the spherical appearance of untreated hepatocytes, and the development of occasional blebs. The appearance of pale staining hydropic cells was indicative of the final stages of cell death. N-Acetylcysteine (6.0 mM) was effective at preventing the depletion of soluble sulfhydryls, the loss of viability, and the ultrastructural effects of 0.5 or 1.0 mM furosemide, suggesting a role for soluble sulfhydryls in the pathogenesis of furosemide hepatotoxicity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3810658&dopt=Abstract
Jpn J Physiol. 1985;35(5):817-30.
Potassium transport in isolated cerebral microvessels from the rat.
Lin JD.
Microvessels have been prepared from the gray matter of a rat brain by a technique involving density gradient centrifugation. A suspension of these vessels, largely capillaries, was incubated in vitro in order to investigate K transport. The flux of K (as 86Rb) into and out of endothelial cells was estimated. Potassium influx was sensitive to temperature and pH of the medium, and was markedly inhibited by 1 mM ouabain (45%). Ouabain did not inhibit K efflux, as anticipated, when Na-K pumps are mainly located on the abluminal plasma membrane of the endothelial cell. The ouabain-sensitive K influx was measured at varying external concentrations of K. The Km of ouabain-sensitive K influx was 2.95 mM, which is similar to the affinity of the transport carrier of K, found in in vivo studies of K efflux from brain to the blood system. Both 1 mM furosemide and 5 mM barium chloride inhibited part of the ouabain-insensitive K influx. Potassium efflux was not influenced by furosemide, but was somewhat reduced by barium chloride. Noradrenalin (10(-3) mM) and histamine (0.1 mM) did not significantly affect the influx of K.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3908762&dopt=Abstract
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