Drugs online research references
Life Sci. 1998;62(20):PL 303-8.
Flufenamic and tolfenamic acids and lemakalim relax guinea-pig isolated trachea by different mechanisms.
Li L, Vapaatalo H, Vaali K, Paakkari I, Kankaanranta H.
Institute of Biomedicine, Department of Pharmacology and Toxicology, University of Helsinki, Finland.
The effects of K+ channel inhibitors on the relaxations induced by flufenamic and tolfenamic acids and lemakalim were examined in guinea-pig isolated trachea precontracted with prostaglandin F2alpha (PGF2alpha, 1 microM). Flufenamic and tolfenamic acids (0.1-33 microM) and lemakalim (0.01-33 microM) relaxed guinea-pig trachea in a concentration-dependent manner. Tetraethylammonium (0.5-2 mM), a nonspecific inhibitor of K+ channels, inhibited the relaxations induced by flufenamic and tolfenamic acids without affecting lemakalim-induced relaxation. Charybdotoxin (ChTX, 33-100 nM), an inhibitor of the large Ca2+-activated K+ channels (BK(Ca)), also inhibited the relaxations induced by flufenamic and tolfenamic acids without affecting lemakalim-induced relaxation. Glipizide (3.3-33 microM), an inhibitor of the ATP-sensitive K+ channels (K(ATP)) inhibited lemakalim-induced relaxation without affecting those induced by flufenamic and tolfenamic acids. Our results indicate that the relaxations of guinea-pig isolated trachea by flufenamic and tolfenamic acids are due to activation of BK(Ca). The relaxant mechanism of flufenamic and tolfenamic acids thus differs from that of lemakalim, an activator of K(ATP).
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9600333&dopt=Abstract
J Immunol. 1998 Jun 1;160(11):5546-53.
Sulfonylureas inhibit cytokine-induced eosinophil survival and activation.
Bankers-Fulbright JL, Kephart GM, Loegering DA, Bradford AL, Okada S, Kita H, Gleich GJ.
Department of Immunology, Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA.
Eosinophils play a key role in the pathogenesis of asthma and other allergic inflammatory diseases. We have previously shown that treatment of eosinophils with lidocaine preferentially inhibits IL-5-induced survival. This inhibition cannot be overcome by increasing concentrations of IL-5 and is not due to the blocking of Na+ channels by lidocaine. Here we report that one class of K+ channel blockers, the sulfonylureas, inhibits eosinophil survival in a manner similar to lidocaine. The sulfonylurea glyburide inhibits eosinophil survival even at high concentrations of IL-5. In contrast, increasing concentrations of IL-3 or granulocyte-macrophage CSF overcome glyburide inhibition. Glyburide also blocks cytokine-induced eosinophil superoxide production. Similar results were seen with the sulfonylureas tolbutamide and glipizide. Interestingly, the effects of glyburide are not antagonized by the ATP-sensitive K+ channel openers cromakalim, pinacidil, or diazoxide. Although Scatchard analysis of [3H]glyburide binding to eosinophil membranes indicated that the high affinity sulfonylurea receptor (SUR1) is not present on eosinophils, human eosinophils do express mRNA homologous to the sulfonylurea receptor family, in keeping with the presence of a sulfonylurea receptor. Finally, coculture of eosinophils with combinations of glyburide, lidocaine, and dexamethasone resulted in synergistic inhibition of cytokine-mediated eosinophil survival and superoxide production. These results have intriguing clinical implications for the treatment of eosinophil-associated diseases.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9605159&dopt=Abstract
Sheng Li Xue Bao. 1997 Oct;49(5):545-50.
[Effect of adenosine on intracellular free calcium in cultured rat hippocampal CA1 neurons during anoxia]
[Article in Chinese]
Wan Q, Wang FZ, Yao H, Liu ZW, Huang YH, Ding AS.
Institute of Basic Medical Sciences, Beijing.
Intracellular free Ca2+ concentration ([Ca2+]i) was measured by laser scanning confocal microscope, using Ca2+ indicator Fluo-3 in cultured hippocampal CA1 neurons isolated from newborn rat. The results showed that acute anoxia induced a rapid increase of [Ca2+]i in hippocampal CA1 neurons, and this increase could be attenuated by 100 mumol/L adenosine significantly. This effect of adenosine could be suppressed by adenosine A1 receptor antagonist CPT or potassium channel blockers, 4-AP and glipizide. These results suggest that adenosine activates 4-AP- or ATP-sensitive potassium channels through A1 receptors, and consequently inhibits the [Ca2+]i elevation in hippocampal neurons during anoxia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9813494&dopt=Abstract
online pharmacies ||
Hair Million herbal formula for hair loss and hair growth ||
Amoxicillin ||
Tramadol ||
Paxil ||
Rx Drugs USA, Prescription Drugs Online Pharmacy ||
Zithromax ||
online pharmacy ||
Antibiotics and prescription medications online literature ||
Antibiotics