Drugs online research references
Eur J Pharmacol. 1994 Jun 2;258(1-2):145-9.
Sulfonylureas mimic glucose in stimulating the uptake of Na+ in pancreatic islets exposed to ouabain.
Saha S, Hellman B.
Department of Medical Cell Biology, University of Uppsala, Sweden.
The increase of sodium in response to ouabain inhibition of the Na+/K+ pump was measured in beta-cell-rich pancreatic islets from ob/ob mice using integrating flame photometry. D-Glucose promoted the uptake of sodium when added at a concentration of 6 mM or above. The hypoglycemic sulfonylurea compound, tolbutamide, mimicked the action of D-glucose in stimulating the sodium uptake at concentrations of 10 microM or above. There was no stimulation beyond that obtained with 20 mM glucose during exposure to 100 microM tolbutamide. Other test substances also affected sodium uptake in a way reflecting known effects on insulin release. Accordingly, the sodium uptake was stimulated with glibenclamide, glipizide, HB 699 (4-[2-(5-chloro-2-methoxybenzamido)ethyl]benzoic acid) and high K+. Sulphonamides (sulfamethazole, sulfadiazine and sulfadoxine) had practically no effect when added at a concentration of 1 mM. Sodium uptake in response to glucose and tolbutamide was antagonized by 400 microM diazoxide or 4 microM tetrodotoxin. It is concluded that both glucose and hypoglycemic sulfonylureas stimulate Na+ entry into the pancreatic beta-cells, a process presumably involving depolarization.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7925593&dopt=Abstract
Naunyn Schmiedebergs Arch Pharmacol. 1994 Jul;350(1):57-62.
Role of ATP-sensitive K+ channels in antinociception induced by R-PIA, an adenosine A1 receptor agonist.
Ocana M, Baeyens JM.
Department of Pharmacology, School of Medicine, University of Granada, Spain.
The influence of several K+ channel-acting drugs on antinociception induced by the adenosine A1 receptor agonist (-)-N6-(2-phenylisopropyl)-adenosine (R-PIA) was evaluated with a tail flick test in mice. The subcutaneous administration of R-PIA (0.5-8 mg/kg) induced a dose-dependent antinociceptive effect. The ATP-sensitive K+ (KATP) channel blocker gliquidone (2-8 micrograms/mouse, i.c.v.) produced a dose-dependent displacement to the right of the R-PIA dose-response line, whereas the KATP channel opener cromakalim (32 micrograms/mouse, i.c.v.) shifted it to the left. Several KATP channel blockers dose-dependently antagonized the antinociceptive effect of R-PIA, the order of potency being gliquidone > glipizide > glibenclamide (i.e., the same order of potency shown by these drugs in blocking KATP channels in neurons). In contrast, the K+ channel blockers 4-aminopyridine and tetraethylammonium did not antagonize the effect of R-PIA. These data suggest that antinociception produced by adenosine A1 receptor agonists is mediated by the opening of ATP-sensitive K+ channels. The present results, together with those of previous studies, further support a role for K+ channel opening in the antinociceptive effect of agonists of receptors coupled to Gi/Go proteins.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7935855&dopt=Abstract
Pharmacology. 1994 Sep;49(3):173-83.
Antagonism of eicosanoid-induced contraction of rat aorta by sulphonylureas.
Zhang H, Cook D.
Department of Surgery, University of Alberta, Edmonton, Canada.
Glibenclamide and other sulphonylureas are extensively used as specific blockers for ATP-dependent potassium channels in vascular smooth muscle. However, glibenclamide has recently been shown to inhibit actions of some prostanoids in vascular smooth muscle. We extend our previous study by examining the relaxant actions of five different sulphonylureas in rat aorta. The inhibitory effects of sulphonylureas on the contractions induced by prostaglandins F2 alpha, E2 and D2, norepinephrine, 5-hydroxytryptamine (5-HT) or potassium chloride (KCl) were examined. Glibenclamide significantly inhibited the contractions produced by prostaglandins F2 alpha, E2 and D2 but was without effect on responses to norepinephrine, 5-HT or KCl. Glimepiride produced significant attenuation of the responses to all agents tested (5-HT, norepinephrine, KCl), although the inhibition of the responses to prostaglandin F2 alpha was most pronounced. Glipizide and tolbutamide had activities similar to that of glibenclamide, while chlorpropamide was devoid of any antagonist action in rat aorta. In rat aorta precontracted with norepinephrine, glibenclamide inhibited the relaxant responses to lemakalim and pinacidil. Thus, in addition to the effect on ATP-dependent potassium channels, glibenclamide inhibits responses to prostaglandins F2 alpha, E2 and D2 but not to other agents. This effect is shared by glimepiride, tolbutamide and glipizide.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7972332&dopt=Abstract
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