Reduction in Turgor Pressure as a Result of Extremely Brief Exposure to CO₂

Abstract

CO₂ depresses water influx into sunflower hypocotyl segments of low water potential; by contrast, it stimulates flux into segments of high water potential. When segments of high potential were placed in a series of mannitol concentrations and allowed to achieve steady rates of water uptake, influx into CO₂-treated tissue in a solution of 3 atm equalled that into control tissue in water. Reasons are given for deducing that a change in internal osmotic concentration (π_i) of the order of 40% would be necessary to account for this result on the basis of π_i. Direct measurements (by cryoscopy and by the minimum volume method) detected no difference in the steady state value for π_i as between CO₂-treated and control tissue. It was therefore concluded that CO₂ had caused some reduction in turgor pressure.

Water uptake into tissue treated with CO₂ for only the first 2 minutes of a 30-minute period was equal to that into tissue treated continuously with CO₂, i.e. 3 times the control value. Ten seconds' CO₂ treatment produced a significant stimulation. When the cycles of treatment were repeated the samples receiving flashes of CO₂ maintained a rate of water uptake superior to that of the control, whereas influx into continuously treated tissue fell below the control value after 1 hour.

CO₂ treatment applied in a moist air chamber stimulated subsequent water influx when the tissue was transferred to water. Fifteen seconds' treatment was sufficient to produce a marked effect. Even when a transition period of 30 minutes in the moist chamber was interposed between CO₂ treatment (5 minutes) and transfer to water, a stimulation was observed. The CO₂ effect could be achieved at zero degrees; 5 minutes' treatment in the moist chamber at zero degrees, followed by a 15-minute transition period at the same temperature, substantially increased subsequent water uptake at 25°.

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