Reduction in Turgor Pressure as a Result of Extremely Brief Exposure to CO(2)

Abstract

CO(2) 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 CO(2)-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 (pi(i)) of the order of 40% would be necessary to account for this result on the basis of pi(i). Direct measurements (by cryoscopy and by the minimum volume method) detected no difference in the steady state value for pi(i) as between CO(2)-treated and control tissue. It was therefore concluded that CO(2) had caused some reduction in turgor pressure.Water uptake into tissue treated with CO(2) for only the first 2 minutes of a 30-minute period was equal to that into tissue treated continuously with CO(2), i.e. 3 times the control value. Ten seconds' CO(2) treatment produced a significant stimulation. When the cycles of treatment were repeated the samples receiving flashes of CO(2) 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.CO(2) 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 CO(2) treatment (5 minutes) and transfer to water, a stimulation was observed. The CO(2) 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 degrees .