Abstract

Guard cell solution osmotic potential changes resulting in the opening and closing of stomata apertures follow an initial influx of potassium ions, their substitution with sucrose molecules and the subsequent reduction of the latter. To provide an insight into the osmotic mechanism of the changes, the new equation for calculating osmotic pressure, which equates the difference between the energy of pure water across a semi-permeable membrane interface with that of solution water, was used to compare the osmotic properties of KCl and sucrose. For sucrose solutions, the effect of the sucrose molecules in increasing the spacing of the solution water was mainly responsible for osmotic potential; this contrasted with K+ + Cl(-) ions where their spacing effect was only a little higher to that of water held to those ions. At solute concentrations giving an osmotic potential level of -3.0 MPa near that of turgid guard cells, the spacing effect on the potential of the unattached solution water molecules caused by sucrose, but in its theoretical absence, was estimated as -2.203 MPa compared with -1.431 MPa for KCl. In contrast, the potential attributed to water molecules firmly held to the K+ + Cl(-) ions was -1.212 MPa versus zero for sucrose. The potential to keep the sucrose molecules in solution was -0.797 MPa compared with -0.357 MPa for KCl. The findings illustrate that the way KCl effects osmotic pressure is very different to that of sucrose. It is concluded that stomata aperture modulation is closely linked to the osmotic properties of its guard cell solution solutes.

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