中文摘要：

运用非损伤微测技术（NMT），研究了短期盐胁迫下胞外ATP（eATP）、H2O2、Ca^2＋与NO对非泌盐红树木榄根系K^＋／Na^＋平衡的调控作用。NaCl（100mmol／L，24h）与等渗甘露醇处理的实验表明，木榄根尖对盐胁迫的响应具有高度的离子特异性。盐胁迫增强了木榄根尖的Na^＋外流，但Na^＋外流被Na^＋／H^＋逆向转运蛋白抑制剂Amiloride和质膜H^＋-ATPase抑制剂Vanadate抑制，表明Na^＋外流源于根尖表皮细胞质膜Na^＋／H^＋逆向转运系统驱动的Na^＋外排。短期盐胁迫处理能诱导木榄根尖K^＋外流，但被氯化四乙胺（TEA，外向K^＋通道抑制剂）明显抑制，证明K^＋外流是由激活的去极化外向型离子通道KORCs介导。胞外ATP（300μmol／L）、H2O2（10mmol／L）、Ca^2＋（10mmol／L）与SNP（NO供体，100μmol／L）均能增加短期盐胁迫下的Na^＋外流，同时抑制K^＋外流。其中，促进Na^＋外流效果较强的是H2O2和Ca^2＋，而Ca^2＋和NO抑制K^＋外流的效果突出。这些实验结果表明，胞外ATP、H2O2、Ca^2＋与NO这4种盐胁迫信使是通过上调木榄根系细胞质膜Na^＋／H^＋逆向转运体系（Na^＋／H^＋逆向转运体和H^＋泵）活性，在促进Na^＋和H^＋逆向跨膜转运的同时，抑制去极化激活的K^＋离子通道来减少盐诱导的K^＋外流。

英文摘要：

Using the noninvasive microtest technique （NMT） , the effects of extracellular ATP （eATP） , hydrogen peroxide （H2O2） , calcium （Ca^2＋ ） and nitric oxide （NO） on root K^＋/Na^＋ homeostasis were investigated in a nonsecretor mangrove species Bruguiera gymnorrhiza under short-term （ST, 24 hours） salt stress （ 100 mmol/L NaCl）. The experiments of NaCl and Mannitol in B. gymnorrhiza roots indicated that there were mainly high ionspecific effects on NaCl-induced ion fluxes in roots. Salt stress resulted in an increased Na^＋ efflux along the root axis of B. gymnorrhiza. However, the salt-enhanced Na^＋ efflux was inhibited by amiloride, a Na ^＋/H ^＋ antiporter inhibitor or sodium orthovanadate, a plasma membrane （PM） H^＋-ATPase inhibitor obviously, suggesting that the Na^＋ efflux was resulted from active Na^＋ exclusion. NaCl treatment caused an evident K^＋ efflux in B. gymnorrhiza, but it was significantly restricted by the K ^＋ channel blocker, TEA, suggesting that the K ^＋ efflux was mediated by K^＋ permeable channels. Exogenously applied eATP （300 μmol/L） , H2O2 （10 mmol/L）, Ca^2＋（10 mmol/L） , or SNP （NO donor, 100 μmol/L） enhanced the salt-elicited Na^＋ efflux but reduced K^＋ efflux under ST treatment. Under salt stress, H202 and Ca^2＋ showed of K^＋ efflux was more pronounced by Ca^2＋ or NO a capacity to exclude Na^＋ , while the inhibition application. In conclusion, our data revealed that eATP, H202, Ca^2＋ , and NO upward regulated Na^＋/H^＋ antiporter and H ^＋ pump, an activity of Na^＋/ H ^＋ antiport system, which compelled the Na^＋/H ^＋ exchange across the plasma membrane and restricted the K ^＋ loss via depolarization-activated K ^＋ channels simultaneously.