Abstract
The relationship between nitric oxide (NO) reduction and the inhibition of abscisic acid (ABA)‐induced stomatal closure by ethylene was analysed. ABA treatment induced NO production and stomatal closure, but ethylene inhibited the effects of ABA on these two parameters. Like 2‐(4‐carboxyphenyl)‐4,4,5,5‐tetramethylimidazoline‐1‐oxyl‐3‐oxide (cPTIO), a specific scavenger of NO, haemoglobin (Hb), the potent scavenger of NO/carbon monoxide (CO) and N G ‐nitro‐L‐Arg‐methyl ester (L‐NAME), an inhibitor of animal nitric oxide synthases (NOS; EC 1.14.13.39), both the ethylene‐releasing compound 2‐chloroethylene phosphonic acid (ethephon, ETH) and 1‐aminocyclopropane‐1‐carboxylic acid (ACC), the immediate precursor of ethylene, were found to inhibit stomatal closure by ABA and to reduce NO levels by ABA in guard cells, indicating that the ethylene‐caused inhibition of ABA‐induced stomatal closure involves a decrease in NO levels in guard cells. In addition, and similar to cPTIO and Hb, ACC/ETH suppressed sodium nitroprusside (SNP)‐induced stomatal closure and NO levels in guard cells treated with SNP in the light. ACC/ETH also reopened stomata that had been closed by ABA and reduced NO levels that had been generated by ABA, showing that ethylene causes NO removal in guard cells. However, the above‐mentioned effect of ACC/ETH was dissimilar to that of L‐NAME, which was incapable of reducing NO levels by SNP or abolishing NO that had been generated by ABA. We suggest that ethylene probably induces NO removal, thereby reducing NO levels in Vicia faba guard cells, and finally inhibits stomatal closure induced by ABA. Furthermore, the pattern of NO reduction caused by ethylene is also discussed.