Drugs online research references
Clin Transplant. 1998 Dec;12(6):553-6.
Glipizide treatment of post-transplant diabetes does not interfere with cyclosporine pharmacokinetics in renal allograft recipients.
Sagedal S, Asberg A, Hartmann A, Bergan S, Berg KJ.
Department of Internal Medicine, National Hospital, Oslo, Norway.
BACKGROUND: Glipizide is an oral antidiabetic drug that has been used in the treatment of post-transplant diabetes mellitus (PTDM). However, a published case report has indicated a possible interaction of glipizide with cyclosporine (CsA) pharmacokinetics in two renal transplant (tx) patients. The aim of this open prospective study was to investigate whether glipizide interacts with CsA pharmacokinetics in renal tx patients with PTDM. METHODS: Eleven renal tx patients (29-74 years of age) with PTDM who received Sandimmun Neoral as part of their immunosuppressive therapy were investigated. No patients had suffered any significant rise in serum creatinine (20%) from any cause over the last 2 wk before the study. Mean S-creatinine was 137 mumol/L (87-220). The mean CsA dose and whole blood concentration remained unchanged during the study. CsA whole blood concentrations were monitored over 12 h in all patients in random order, both on and off glipizide treatment. Blood samples were drawn immediately before the morning dose of CsA was given (trough) and 0.5, 1, 1.5, 2, 3, 4, 6 and 12 h after administration. RESULTS: Whole blood trough CsA concentration was not altered by glipizide treatment, 256 +/- 76 micrograms/L off and 242 +/- 73 micrograms/L (mean +/- SD) with glipizide coadministration. The area under the curve (AUC) and terminal half-life of CsA remained unchanged with glipizide treatment: 6391 +/- 1483 micrograms/L per h and 7.3 +/- 1.5 h without; and 6279 +/- 1601 micrograms/L per h and 7.1 +/- 1.8 h with glipizide, respectively. No change in the CsA peak concentration (Cmax) was observed: 1507 +/- 406 micrograms/L without and 1469 +/- 538 micrograms/L with glipizide coadministration. CONCLUSION: CsA pharmacokinetics is not significantly altered by glipizide coadministration.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9850449&dopt=Abstract
koki.hu
In this study the role of ATP-sensitive K(+) channels (K(ATP) channels) in the A(1) receptor mediated presynaptic inhibitory modulation of acetylcholine release was investigated in the rat hippocampus. N(6)-Cyclohexyladenosine (CHA), the selective A(1)-adenosine receptor agonist, reduced concentration-dependently the stimulation-evoked (2 Hz, 1 ms, 240 shocks) [3H]acetylcholine ([3H]ACh) release, from in vitro superfused hippocampal slices preloaded with [3H]choline, an effect prevented by the selective A(1) receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). By themselves, neither K(ATP) channel openers, i.e. diazoxide, pinacidil and cromakalim, nor glibenclamide and glipizide, the inhibitors of K(ATP) channels, exerted a significant effect on the resting and evoked release of [3H]ACh. Glibenclamide and glipizide (10-100 microM) completely prevented the inhibitory effect of 0.1 microM CHA and shifted the concentration response curve of CHA to the right. 4-Aminopyridine (10-100 microM), the non-selective potassium channel blocker, increased the evoked release of [3H]ACh, but in the presence of 4-aminopyridine, the inhibitory effect of CHA (0.1 microM) still persisted. Oxotremorine, the M(2) muscarinic receptor agonist, decreased the stimulation-evoked release of [3H]ACh, but its effect was not reversed by glibenclamide. 1,3-Diethyl-8-phenylxanthine (DPX), the selective A(1)-antagonist, effectively displaced [3H]DPCPX in binding experiments, while in the case of glibenclamide and glipizide, only slight displacement was observed. In summary, our results suggest that K(ATP) channels are functionally coupled to A(1) receptors present on cholinergic terminals of the hippocampus, and glibenclamide and glipizide, by interacting with K(ATP) channels, relieve this inhibitory neuromodulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11166687&dopt=Abstract
Acta Diabetol Lat. 1976 Jan-Apr;13(1-2):20-4.
Comparison of the effects of leucines, non-metabolizable leucine analogues and other insulin secretagogues on the activity of glutamate dehydrogenase.
Gylfe E.
Glutamate dehydrogenase (GLDH) from bovine liver was employed in model system for testing a possible role of GLDH in insulin release. The ability of different insulin secretagogues to stimulate the activity of the diethylstilbestrol-inhibited enzyme was tested. The two insulin-releasing amino acids, L-leucine and its non-metabolizable analogue 2-aminobicyclo(2, 2, 1)heptane-2-carboxylic acid [b(--)-BCH], were the best stimulators of GLDH activity. The non-secreting stereoisomers, D-leucine and b(+)-BCH, were less effective. Glucose, L-arginine and the leucine metabolite alpha-ketoisocaproic acid lacked significant effects on GLDH activity. Small and diverging effects were obtained with sulfonvlurea compounds: whereas carbutamide caused slight stimulation, tolbutamide and glipizide had no effect, and glibenclamide was an inhibitor. The specificity of the insulin-releasing amino acids L-leucine and b(--)-BCH in stimulating GLDH activity makes it tempting to speculate about a connection between allosteric regulation of pyridine nucleotide-dependent enzymes and insulin release.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=987682&dopt=Abstract
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