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Lysine transport by in vitro distal rabbit ileum has been investigated by determining (a) transmural fluxes across short-circuited segments of the tissue; (b) accumulation by mucosal strips; and (c) influx from the mucosal solution across the brush border into the epithelium. Net transmural flux of lysine is considerably smaller than that of alanine. However, lysine influx across the brush border and lysine accumulation by mucosal strips are quantitatively comparable to alanine influx and accumulation. Evidence is presented that the "low transport capacity" of rabbit ileum for lysine is due to: (a) a carriermediated process responsible for efltux of lysine out of the cell across the serosal and/or lateral membranes that is characterized by a low maximal velocity; and (b) a high "backflux" of lysine out of the cell across the mucosal membrane. A possible explanation for the latter observation is discussed with reference to the relatively low Na dependence of lysine transport across the intestinal brush border.The ability of small intestine to transport neutral amino acids from a lower concentration in the mucosal solution to a higher concentration in the serosal solution was first demonstrated by Wiseman in 1951 (1). Since then the transport of neutral amino acids b y in vitro preparations of mammalian small intestine has been the subject of numerous investigations and has been described in considerable detail. In 1961, Hagihira et al. (9) demonstrated transport of the basic amino acids across everted sacs of hamster small intestine against a concentration difference using low initial concentrations in the mucosal and serosal fluids. These investigators noted that the maximal rates of transport of the basic amino acids were only 5 -1 0 % of the rates of transport of neutral amino acids and concluded that the earlier failure to demonstrate net transport in the presence of high initial mucosal and serosal concentrations (3) could be attributed to this small transport "capacity." Since 1961, there have been relatively few studies dealing with the characteristics of basic amino acid transport across in vitro small intestine, but nevertheless the initial observations and conclusions of Hagihira et al. have been substantially confirmed (4-8).This "small transport capacity" of in vitro small intestine for basic amino acids raises several questions.

The rat intestinal imino acid carrier is chloride independent, while in guinea pig and rabbit intestine it is chloride dependent. While non-alpha-amino acids do not significantly interact with guinea pig and rabbit imino acid carriers, inhibition studies had indicated that in rat small intestine beta-alanine, gamma-aminobutyric acid (GABA), and probably taurine might be transported by the imino acid carrier. The present study of rat jejunum demonstrates that the half-maximal activation concentration of beta-alanine (K1/2 beta-Ala) is identical to its inhibition constant (Ki beta-Ala) against GABA, that K1/2GABA is identical to KiGABA against beta-alanine, that proline and sarcosine have identical values of Ki against beta-alanine and GABA, and that Ki of beta-alanine and proline against sarcosine are equal to their K1/2 values. Taurine inhibits the transport of beta-alanine, and 300 mM proline and beta-alanine reduce the transport of taurine measured at 80 mM taurine to the level expected for the diffusive contribution, corresponding to Ki values equal to those against sarcosine. Thus the rat imino acid carrier is the principal carrier of taurine and the only carrier of beta-alanine and GABA. It is also demonstrated that alpha-amino-monocarboxylic acids with side chains in excess of one methyl group do not significantly interact with the imino acid carrier, and the lack of stereospecificity is confirmed.

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