Abstract
The pressure/volume relationship of toad urinary bladders was measured from 0 to 50 cmH2O. Optimal bladder capacity was derived by extrapolation of the pressure/volume curve to a pressure of 0 cmH2O. The compliance of the bladder wall was calculated from the slope of the pressure/volume curve at intraluminal pressures above 10 cmH2O. Neither vasopressin nor atropine had any effect on bladder wall compliance. Bladders filled with one-fifth strength Ringer fluid and suspended in full-strength Ringer lost weight at 0.02 (at half-optimal capacity), 0.08 (at optimal capacity), and 0.26 mg.min-1.cm-2 (at supra-optimal capacity, 25 cmH2O) in the absence of vasopressin. With 20 mU/ml vasopressin, bladders lost weight at 1.08 (at half-optimal capacity), 1.55 (at optimal capacity), and 1.74 mg.min-1.cm-2 (at supra-optimal capacity, 25 cmH2O). When bladder wall tension was raised from 2,102 to 28,383 dyn/cm, the permeability to [14C]mannitol increased from 8 X 10(-7) to 39 X 10(-7) cm/s. Electron microscopy of bladders fixed at a wall tension of 17,572 dyn/cm showed flattening of the microvilli, rupture of the apical cell membranes of some granular and mitochondria-rich epithelial cells, but no obvious alteration in the tight junctions. This study suggests that stretching the apical plasma membrane to the point at which it ruptures in some cells does not alter the capacity of vasopressin to induce its characteristic increase in permeability to water of this membrane.
Publisher
American Physiological Society
Cited by
4 articles.
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