Vasopressin increases water permeability by inducing pores

Abstract

Vasopressin is thought to increase the water permeability of the luminal membrane of distal urinary epithelia either by enhancing the solubility or diffusion of water in the lipid phase¹ or by inducing aqueous pores². Measurement of the permeability to water and small solutes in different experimental conditions should allow the distinction between these two modes of water transport^1–9, but because of technical difficulties (for instance the effect of unstirred layers^3–6) or conceptual problems (in the case of activation energy measurements^7–9) the interpretation of many of these methods is in question. We present here a new approach to this problem using proton conductance of the membrane as a probe for the presence of aqueous channels. Protons travel in free solution by jumping from one water molecule to another¹⁰. If vasopressin induces aqueous pores, it should also increase proton permeability, as protons will be able to jump from a water molecule in the bulk solution to another in the pore. However, if vasopressin changes water permeability by increasing membrane fluidity the proton conductance should not increase as the dielectric constant of even very fluid lipids is low, leading to extremely low solubility of ions in the lipid¹¹. We found that vasopressin increased the proton permeability of the luminal membrane of the toad urinary bladder and conclude that this hormone increases water permeability by inducing aqueous pores rather than by increasing lipid fluidity. Proton conductance may be of use in determining the existence and properties of other aqueous channels.