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These experiments were intended to evaluate the antidiuretic hormone (ADH)-dependent reflection coefficients of urea, sucrose, and NaCl in cortical and outer medullary collecting tubules isolated from mammalian kidney. In one group of experiments, the ADH-dependent osmotic water flows, when the perfusing solutions contained hypotonic NaCl solutions, were indistinguishable from control observations when either urea or sucrose replaced, in part, NaCl in isotonic bathing solutions (cortical collecting tubules). Similarly, both in cortical and outer medullary collecting tubules exposed to ADH, there was zero net osmotic volume flow when a portion of the NaCl in the bathing and/or perfusing solutions was replaced by either sucrose or urea, so long as the perfusing and bathing solutions were isosmolal. Taken together, these observations suggest that the ADH-dependent reflection coefficients of NaCl, urea, and sucrose, in these tubules, were identical. Since the effective hydrodynamic radii of urea and sucrose are, respectively, 1.8 and 5.2 A, it is likely that sigma(i), for urea, sucrose, and NaCl, was unity. In support of this, the diffusion permeability coefficient (P(Di) cm sec(-1)) of urea was indistinguishable from zero. Since the limiting sites for urea penetration were the luminal interfaces of the tubules, these data are consistent with the view that ADH increases diffusional water flow across such interfaces.

These experiments were intended to evaluate the effects of antidiuretic hormone (ADH) on dissipative water transport in cortical collecting tubules isolated from rabbit kidney. In the absence of ADH, the osmotic (P(f), cm sec(-1)) and diffusional (P(DW) cm sec(-1)) water permeability coefficients were, respectively, 6+/-6 and 4.7+/-1.3 (SD). When ADH was added to the bathing solutions, P(f) and P(DW) rose to, respectively, 186+/-38 and 14.2+/-1.6 (SD). In the absence of ADH, the tubular cells were flat and the lateral intercellular spaces were closed when the perfusing and bathing solutions were, respectively, hypotonic and isotonic; in the presence of ADH, the cells swelled and the intercellular spaces dilated. These data suggest that ADH increased the water permeability of the luminal membranes of the tubules. It was possible that the ADH-dependent P(f)/P(DW) ratio was referable to the resistance of the epithelial cell layer (exclusive of luminal membranes) to water diffusion (R(DW), sec cm(-1)). Such a possibility required that R(DW) be approximately 650, i.e., approximately 25-fold greater than in an equivalent thickness of water. To test this view, it was assumed that R(Di) values for lipophilic solutes in lipid bilayer membranes and in luminal membranes were comparable. In lipid bilayer membranes, R(Di) was substantially less than 90 sec cm(-1) for pyridine, n-butanol, and 5-hydroxyindole. In renal tubules, R(Di) for these solutes ranged from 795 to 2480 with and without ADH. It was assumed that, in the tubules, R(Di) was referable to cellular constraints to diffusion; for these solutes, the latter were 12-25 times greater than in water. Accordingly, it is possible that the ADH-dependent P(f)/P(DW) ratio was also due to cellular constraints to diffusion.