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The possible contribution of K+ channel activation to airway smooth muscle relaxation induced by vasoactive intestinal peptide (VIP) and atrial natriuretic peptide (ANP) was investigated in isolated guinea-pig trachea. Concentration-relaxation (CR) curves were assessed in preparations precontracted by 30 mM K+, 124 mM K+ or histamine either alone or in the presence of a K+ channel blocker: iberiotoxin (IbTX), glipizide, tetraethylammonium (TEA) or Ba2+. VIP completely relaxed contractions induced by histamine but had a lower effectiveness against those induced by 30 mM K+ and 124 mM K+. IbTX and TEA shifted the CR curve for VIP 5 and 14 times to the right, respectively. Glipizide and Ba2+ did not significantly antagonize the action of VIP. ANP relaxed contractions induced by histamine and 30 mM K+ but failed to relax those elicited by 124 mM K+. IbTX and TEA shifted the CR curve for ANP 8 and 46 times to the right, respectively. Glipizide and Ba2+ suppressed the maximal effect produced by ANP, and glipizide also shifted the CR curve to the left. The K+ channel opener levcromakalim relaxed tracheal contractions induced by histamine and 30 mM K+ but not those induced by 124 mM K+. Glipizide caused a 5-fold rightward shift of the CR curve for levcromakalim whereas IbTX shifted the curve to the left and increased the maximal relaxant effect. The Ca2+ channel blocker isradipine completely relaxed contractions induced by 30 mM K+ and 124 mM K+ but only partially relaxed those contracted by histamine. All four K+ channel blockers increased the maximal relaxant effect and shifted the CR curve for isradipine to the left. The results suggest that airway smooth muscle relaxation produced by VIP and ANP involves activation of large-conductance Ca(2+)-activated K+ channels (BKCa) and further that ANP may possibly activate other types of K+ channels additional to BKCa.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9042598&dopt=Abstract
Naunyn Schmiedebergs Arch Pharmacol. 1997 Feb;355(2):141-9.
Sulphonylurea binding in rat isolated glomeruli: pharmacological characterization and dependence on cell metabolism and cytoskeleton.
Metzger F, Loffler C, Quast U.
Department of Pharmacology, University of Tubingen, Germany.
The kidney is endowed with ATP-sensitive K+ channels (KATP channels) both at the vascular and at the epithelial level. In this study we have characterized the binding of the sulphonylurea glibenclamide, the most widely used blocker of KATP channels, in rat isolated glomeruli. In metabolically intact glomeruli, 3H-glibenclamide labelled two different binding components with affinities of 47 +/- 12 nM and 10 +/- 1 microM and estimated binding capacities of 1.2 +/- 0.1 and 501 +/- 11 pmol/mg protein, respectively. 3H-glibenclamide binding was inhibited differentially by other sulphonylureas (tolbutamide, glibornuride, gliquidone and glipizide) and benzoic acid analogues such as meglitinide, AZ-DF 265 and UL-DF 9. Sulphonylureas interacted with the high affinity component and, in some cases, also with the low affinity component whereas the benzoic acid derivatives inhibited exclusively low affinity glibenclamide binding. Severe metabolic stress affected both components of glibenclamide binding by shifting high affinity binding to the right and reducing the capacity of the low affinity component. Disruption of the cytoskeletal actin filaments by cytochalasin B and D mimicked the effect of metabolic stress on the high affinity component but left the low affinity component unchanged. In crude membranes, the affinity of the first component was again reduced and a major loss of the low affinity sites was observed. The data show that the two binding components of glibenclamide binding in rat isolated glomeruli have very different properties. The high affinity component is not recognized by the benzoic acid derivatives; its affinity is modulated by cell metabolism and the actin component of the cytoskeleton. The low affinity sites are, in their majority, cytosolic. The function and cellular localization of the high affinity sites are under further study.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9050005&dopt=Abstract
In Vivo. 1997 Jan-Feb;11(1):103-7.
Phototoxicity to sulphonamide derived oral antidiabetics and diuretics. Comparative in vitro and in vivo investigations.
Selvaag E, Anholt H, Moan J, Thune P.
Department of Dermatology, Ullevaal Hospital, University of Oslo, Norway.
The oral antidiabetics chlorpropamide, glibenclamide, glipizide, gliquiudone, glymidine, tolazamide and tolbutamide, and the diuretics bemetizide, bendroflumethiazide, benzylhydrochlorothiazide, bumetanide, butizide, chlortalidone, furosemide, hydrochlorothiazide, hydroflumethiazide, indapamide, piretanide, polythiazide, trichlormethiazide, and xipamide were investigated for potential phototoxicity in vitro using a cell culture model, and in vivo in hairless mice. After exposure to broad band UVA, the majority of the substances tested in vitro yielded a phototoxic action leading to loss of culture forming ability. In vivo, all tested substances induced edema or ulceration, and lead to a significantly increase in skin fold thickness of the mouse skin. In all, a number of substances not described to induce clinical photosensitivity nor phototoxicity in vitro or in vivo were detected in our testing. When determining potential photosensitizers, it seems important to utilize different test methods, as not all substances will exhibit action in a given assay.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9067780&dopt=Abstract
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