Please do not adjust margins There are two putative H + /Cl -symport mechanisms. The first involves protonation of a neutral receptor and subsequent binding of chloride as a neutral complex, followed by the diffusion of the neutral free receptors back across the membrane to complete the transport cycle. The naturally occurring anionophore prodigiosin has been shown to operate via this mechanism. Transport mediated by this process should be unaffected by membrane potential, as it involves the diffusion of neutral species only. A second mechanism arises when an anionophore transports chloride as a negatively charged receptor•chloride complex and diffuses back as a negatively charged deprotonated species or complex with deprotonated fatty acids. If the anionophore cannot diffuse through the membrane as a neutral anion-free receptor due to strong binding to phosphate headgroups, symport via this mechanism should be attenuated by the generation of a membrane potential because this should inhibit the diffusion of either one of the negatively charged species or complex. The bis-urea compounds 1-5 all showed an attenuation in transport rate when either a positive or negative membrane potential was applied (Figure ). This provides evidence that H + /Cl -symport is facilitated by a non-uniport mechanism, likely due to strong interactions with the phosphate headgroups as proposed in previous voltage-dependent transport studies. The possibility of tautomerism of the deprotonated form of the receptor may also favour this mechanism, as this would delocalise the negative charge over a greater portion of the molecule and allow it to diffuse through the membrane more easily.