Stomatal Responses to Sulphur Dioxide and Vapour Pressure Deficit

Abstract

Stomatal conductances (g_s) 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 g_s in V. faba. This response persisted throughout the exposure (3 d). The increase in g_s, 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 g_s. When vpd was varied, g_s 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 g_s at all vpd values. g_s 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 g_s, but, above a certain value of vpd, depending on species, g_s 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.