Stomatal Responses to Sulphur Dioxide and Vapour Pressure Deficit

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Abstract
Stomatal conductances (gs) of plants of Vicia faba, Raphanus sativus, Phaseolus vulgaris, Heilanthus annuus, and Nicotiana tabacum were measured in chambers containing either clean air or air containing between 18 and 1000 parts 10−9 SO2 at water vapour pressure deficits (vpd) ranging from 1·0 to 1·8 kPa. When vpd was low (2 induced rapid and irreversible increases in gs in V. faba. This response persisted throughout the exposure (3 d). The increase in gs, 20–30% compared with clean air, was independent of SO2 concentration up to 350 parts 10−9 Stomatal conductances of polluted plants at night were greater than controls. When stomata were closed before exposure to SO2, there was no effect on gs. When vpd was varied, gs of unpolluted plants of P. vulgaris showed no response, but that of R. sativus increased slightly with increasing vpd. In both species exposure to SO2 caused an increase in gs at all vpd values. gs of unpolluted plants of V. faba, H. annuus, and N. tabacum decreased with increasing vpd. At low vpd values exposure to SO2 in these species caused an increase in gs, but, above a certain value of vpd, depending on species, gs decreased with exposure to SO2. It is postulated that SO2, once in the substomatal cavity, enters the stomatal complex via adjacent epidermal cells and at low concentrations leads to a reduction in turgor in these cells and consequently to stomatal opening. In vpd-sensitive species, increased transpiration from guard cells or epidermal cells adjacent to the stomata induced by SO2 may lead to stomatal closure at large vpd levels. Stomatal sensitivity to vpd in such cases may be enhanced because adjacent epidermal cell turgor is lowered by SO2. At high SO2 concentrations direct disruption of guard cell structure may lead to a loss of turgor and stomatal closure.