Cytosolic free calcium and intracellular pH in ischemic and drug-induced acute renal failure.

1.细胞缺血时细胞内游离钙([Ca~(2+)]i)和细胞内pH(Phi)的变化加入氰化物和2-脱氧-D-葡萄糖后，[Ca~(2+)]i升高，Phi降低(DELTApH=-0.35)。维拉帕米(10^&lt；-4；M)或EGTA(2 MM)显著抑制[Ca~(2+)]i的升高，并降低phi(DELTApH=-0.65)。将胞外pH从7.8降至6.4，可抑制代谢抑制剂诱导的[Ca^&lt；2+&gt；]i升高。与pH 7.4.2孵育的细胞相比，在pH 6.5时或与维拉帕米共同孵育的IMCD细胞对缺血损伤具有保护作用。环孢素对LLC-PK细胞[Ca~(2+)]i的影响：环孢素对LLC-PK细胞[Ca~(2+)]i无影响。氧化应激对培养的大鼠IMCD细胞的作用：叔丁基氢过氧化氢(TBHP)(5 MM)可使培养的大鼠IMCD细胞[Ca~(2+)]i升高，60min时细胞存活率降至26I，-lt；正负-8.9%。EGTA(2 MM)或维拉帕米(10^&lt；-4&gt；M)可显著抑制TBHP引起的[Ca~(2+)]i升高。EGTA和维拉帕米都提供了显著的保护作用(细胞存活率。TBHP+EGTA：61.7%+-13.1%，TBHP+维拉帕米：64.7&lt；+-5.5%，TBHP：26.7&lt；+-8.9%。P&lt；0.001；。将细胞外pH从7.4降至6.6可钝化TBHP引起的[Ca^&lt；2+&gt；]升高，并保护细胞损伤(细胞活力。在pH 6.6时：66.2&lt；正负15.7%)

1. Cytosolic free calcium ([Ca^<2+>]i) and intracellular pH(pHi) during cell ischemiaThe effect of ischemia on [Ca^<2+>]i and pHi was determined in cultured rat inner medullary collecting duct (IMCD) cells exposed to NaCN (5mM) and 2-deoxy-D-glucose (5mM). After the addition of cyanide plus 2-deoxy-D-glucose, [Ca^<2+>]i rose and pHi decreased (DELTApH=-0.35). Verapamil (10^<-4>M) or EGTA (2mM) significantly blunted the rise in [Ca^<2+>]i, and decreased pHi moreover (DELTApH=-0.65). Lowering extracellular pH from 7.8 to 6.4 inhibited the rise in [Ca^<2+>]i induced by metabobic inhibitors. At pH 6.5, or with verapamil IMCD cells were protected against ischemic injury as compared with cells incubated at pH 7.4.2. Effect of cyclosporin on [Ca^<2+>]i.Cyclosporin (10^<-8>M) had no effect on [Ca^<2+>]i in LLC-PK, cells.3. Oxidative stress in cultured rat IMCD cells : role of Ca^<2+>.Tert-Butyl Hydroperoxide (TBHP) (5mM) increased [Ca^<2+>]i and reduced IMCD cells viability to 26i, <plus-minus>8.9% at 60min. The increase in [Ca^<2+>]i induced by TBHP was significantly inhibited by EGTA (2mM) or verapamil (10^<-4>M). Both EGTA and verapamil provided significant protection (cell viability. TBHP+EGTA : 61.7<plus-minus>13.1%, TBHP + verapamil : 64.7<plus-minus>5.5%, TBHP : 26.7 <plus-minus>8.9%. P<0.001>. Lowering extracellular pH from 7.4 to 6.6 blunted the rise in [Ca^<2+>] induced by TBHP and protected cell injury (Cell viability. at pH 6.6 : 66.2 <plus-minus> 15.7%)