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Neuroreport. 1998 Feb 16;9(3):447-53.
Effects of K+ channel blockers on the anoxic response of CNS myelinated axons.

Stys PK, Hubatsch DA, Leppanen LL.

Ottawa Civic Hospital Loeb Medical Research Institute, Division of Neuroscience, University of Ottawa, Ont, Canada.

Compound action potentials (CAPs) from adult rat optic nerves were recorded in vitro. The area under the CAP was compared before and after 1 h anoxia/reoxygenation. Resting compound membrane potential was measured using the cold grease-gap technique. The acute reduction of CAP magnitude by anoxia was unaffected by TEA (20 mM), 4-AP (300 microM), or the KATP blockers glibenclamide (300 microM) and tolbutamide (2 mM). Neither these K+ channel blockers, nor glipizide (100 microM) or the KATP activator diazoxide (500 microM) altered post-anoxic CAP area recovery. In contrast, although Cs+ (5 mM) accelerated anoxic CAP failure and membrane depolarization, this cation significantly increased CAP area recovery post-anoxia from 22+/-10% (s.d.) to 60+/-22% (p < 0.0001). The unique effects of Cs+ suggest that inward rectifier channels may play an important role in the induction of anoxic injury in optic nerve axons.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9512388&dopt=Abstract




Br J Pharmacol. 1998 Mar;123(6):1103-10.
Characterization of K(ATP) channels in intact mammalian skeletal muscle fibres.

Barrett-Jolley R, McPherson GA.

Ion Channel Group, Cell Physiology and Pharmacology, Leicester University, UK.

1. The aim of this study was to characterize the K(ATP) channel of intact rat skeletal muscle (rat flexor digitorum brevis muscle). Changes in membrane currents were recorded with two-electrode voltage-clamp of whole fibres. 2. The K(ATP) channel openers, levcromakalim and pinacidil (10-400 microM), caused a concentration-dependent increase in whole-cell chord conductance (up to approximately 1.5 mScm(-2)). The activated current had a weak inwardly rectifying current-voltage relation, a reversal potential near E(K) and nanomolar sensitivity to glibenclamide--characteristic of a K(ATP) channel current. Concentration-effect analysis revealed that levcromakalim and pinacidil were not particularly potent (EC50 approximately 186 microM, approximately 30 microM, respectively), but diazoxide was completely inactive. 3. The ability of both classical K(ATP) channel inhibitors (glibenclamide, tolbutamide, glipizide and 5-hydroxydecanoic acid) and a number of structurally related glibenclamide analogues to antagonize the levcromakalim-induced current was determined. Glibenclamide was the most potent compound with an IC50 of approximately 5 nM. However, the non-sulphonylurea (but cardioactive) compound 5-hydroxydecanoic acid was inactive in this preparation. 4. Regression analysis showed that the glibenclamide analogues used have a similar rank order of potency to that observed previously in vascular smooth muscle and cerebral tissue. However, two compounds (glipizide and DK13) were found to have unexpectedly low potency in skeletal muscle. 5. These experiments revealed K(ATP) channels of skeletal muscle to be at least 10x more sensitive to glibenclamide than previously found; this may be because of the requirement for an intact intracellular environment for the full effect of sulphonylureas to be realised. Pharmacologically, K(ATP) channels of mammalian skeletal muscle appear to resemble most closely K(ATP) channels of cardiac myocytes.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9559893&dopt=Abstract




Eur J Pharmacol. 1998 Feb 19;343(2-3):225-32.
Sulfonylurea effects on acid and pepsinogen secretion in isolated rabbit gastric glands.

Del Valle JC, Olea J, Pereda C, Gutierrez Y, Feliu JE, Rossi I.

Servicio de Endocrinologia Experimental, Clinica Puerta de Hierro, Facultad de Medicina, Universidad Autonoma de Madrid, Spain.

The influence of different sulfonylureas on the rate of acid and pepsinogen secretion was studied in isolated rabbit gastric glands. Neither tolbutamide (10-500 microM), chlorpropamide (10-500 microM), glibenclamide (1-50 microM) nor glipizide (1-50 microM) exerted a secretory effect. In contrast, gliquidone caused a marked and dose-dependent stimulation of acid production in gastric glands incubated under basal conditions and potentiated the stimulatory effect of both histamine and carbachol. Gliquidone also increased the rate of pepsinogen release in gastric glands incubated either under basal conditions or in the presence of cholecystokinin-octapeptide or isoproterenol. The secretory effects of gliquidone were associated with a significant increase in the glandular content of cyclic AMP, caused by a competitive inhibition of low-Km cyclic AMP phosphodiesterase. Our results indicate that, among the assayed sulfonylureas, only gliquidone, in the micromolar range, stimulates acid and pepsinogen secretion through a cyclic AMP-dependent mechanism.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9570471&dopt=Abstract












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