Mammalian spermatozoa are not able to fertilize an oocyte upon ejaculation. To gain fertilizing ability, spermatozoa must, either in vivo or in vitro, undergo a process termed capacitation. Since a reliable marker for capacitation does not exist, it is considered that this process is completed when the spermatozoa are able to undergo acrosomal x intestinal mucosa which might require tandem signaling events for this process is the presence of a vascular countercurrent arrangement in the subepithelial compartment. As happens for absorbed solutes, this countercurrent phenomenon may distort transepithelial solute gradient. For example, perfusion of mammalian intestinal loops in vivo with solutions containing fMLP was previously found to induce neutrophil attachment to endothelial cells and structurally defined endothelial activation, but failed to elicit directed migration across the lamina propria (Madara, unpublished observations), suggesting that directed migration may require a more stable gradient than that afforded by the usual soluble signals. For example, once present in inflamed tissue, IL-8 is likely to retain its biological activity for several hours, as shown by local intradermal administration in animals and humans. In contrast to Il-8, chemokines such as fMLP or LTB4 are degraded rapidly by oxidation or hydrolysis. Fertilization is a very complex phenomenon, involving sequential interactions between the fertilizing spermatozoon and cumulus oophorus, ZP, and oolemma. The AR may be playing a key role in penetration of spermatozoa through these egg vestments.