PubMed · 5773520
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L C Isaacson. 1969. Urinary composition in calcific nephrolithiasis.. https://pubmed.ncbi.nlm.nih.gov/5773520/
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Using the MIN6 B-cell line, we investigated the hypothesis that miniglucagon, the C-terminal () fragment processed from glucagon and present in pancreatic A cells, modulates insulin release, and we analyzed its cellular mode of action. We show that, at concentrations ranging from 0.01 to 1000 pM, miniglucagon dose-dependently (ID50 = 1 pM) inhibited by 80-100% the insulin release triggered by glucose, glucagon, glucagon-like peptide-1-(7-36) amide (tGLP-1), or glibenclamide, but not that induced by carbachol. Miniglucagon had no significant effects on cellular cAMP levels. The increase in 45Ca2+ uptake induced by depolarizing agents (glucose or extracellular K+), by glucagon, or by the Ca2+channel agonist Bay K-8644 was blocked by miniglucagon at the doses active on insulin release. Electrophysiological experiments indicated that miniglucagon induces membrane hyperpolarization, probably by opening potassium channels, which terminated glucose-induced electrical activity. Pretreatment with pertussis toxin abolished the effects of miniglucagon on insulin release. It is concluded that miniglucagon is a highly potent and efficient inhibitor of insulin release by closing, via hyperpolarization, voltage-dependent Ca2+ channels linked to a pathway involving a pertussis toxin-sensitive G protein.
A single channel current was recorded from mitoplasts (i.e., inner mitochondrial membrane) of the human glioma cell line LN229 using patch-clamp techniques in the mitoplast-attached mode. We frequently found a 295 +/- 18 pS channel that showed a straight i-E relation in the range +/-60 mV in 150 mM KCl solutions on either side of the mitoplast. If KCl in the bath was exchanged against NaCl, outward currents were undetectable, indicating potassium selectivity. Channel activity determined as open probability increased with increasing Ca2+ concentrations (EC50 = 0.9 microM at 60 mV). Open probability was voltage dependent. An e-fold increase of time spent in the open state was induced by a depolarization of 10.5 mV. Open probability was decreased by charybdotoxin concentration and voltage dependently (EC50 = 1.4 nM). In conclusion, we show for the first time that the inner mitochondrial membrane in human glioma cells contains a calcium-dependent K channel of the BK-type.
BACKGROUND: Hydrogen peroxide (H2O2) and reactive oxygen species are implicated in inflammation, ischemia-reperfusion injury, and atherosclerosis. The role of ion channels has not been previously explored. METHODS AND RESULTS: K+ currents and membrane potential were recorded in endothelial cells by voltage- and current-clamp techniques. H2O2 elicited both hyperpolarization and depolarization of the membrane potential in a concentration-dependent manner. Low H2O2 concentrations (0.01 to 0.25 micromol/L) inhibited the inward-rectifying K+ current (KIR). Whole-cell K+ current analysis revealed that H2O2 (1 mmol/L) applied to the bath solution increased the Ca2+-dependent K+ current (KCa) amplitude. H2O2 increased KCa current in outside-out patches in a Ca2+-free solution. When catalase (5000 micro/mL) was added to the bath solution, the outward-rectifying K+ current amplitude was restored. In contrast, superoxide dismutase (1000 u/mL) had only a small effect on the H2O2-induced K+ current changes. Next, we measured whole-cell K+ currents and redox potentials simultaneously with a novel redox potential-sensitive electrode. The H2O2-mediated KCa current increase was accompanied by a whole-cell redox potential decrease. CONCLUSIONS: H2O2 elicited both hyperpolarization and depolarization of the membrane potential through 2 different mechanisms. Low H2O2 concentrations inhibited inward-rectifying K+ currents, whereas higher H2O2 concentrations increased the amplitude of the outward K+ current. We suggest that reactive oxygen species generated locally increases the KCa current amplitude, whereas low H2O2 concentrations inhibit KIR via intracellular messengers.