It has been proposed that contact between the rat blastocyst and the endometrium is conditioned by like electrical charges on their membranes. Clemetson, Mallikarjuneswara, Moshfeghi, Carr & Wilds (1970) and Clemetson, Kim, Mallikarjuneswara & Wilds (1972) presented data purporting to show that treatment of rats with oestrogen or with progesterone could modify the potential of the endometrium and influence contact. Clemetson et al. (1970) stated that 'the high negative membrane potential under the influence of progesterone may be the cause of delayed implantation by repelling the negatively charged blastocyst. Conversely, the lowering of the negative membrane potential under oestrogen treatment could remove or reduce this repelling action and favour contact necessary for attachment and subsequent implantation.' The mechanism by which these changes in potential occurred was attributed to hormonally controlled alterations in the concentrations of sodium and potassium ions in the luminal and intracellular fluids of the endometrial cells. Clemetson et al. (1972) argued that 'the high uterine fluid potassium ion concentration at the time of normal implantation is essential to reduce the membrane potential of the endometrial epithelium in order to allow the negatively charged blastocyst to make contact with it'. Careful scrutiny of the data reveals, however, that their hypotheses are based on one erroneous and one inappropriate assumption. In both papers the potential differences across the luminal membranes of the endometrial cells (transluminal membrane p.d.) were calculated for each hormonal treatment from measured concen¬ trations of sodium and potassium ions in the luminal fluid and from hypothetical values for the intracellular fluid of endometrial cells based on data obtained in the rabbit. The values were inserted into a modified Goldman equation and potential differences (p.d.) of negative polarity were calculated. The polarity of these calculated p.d. revealed that the intracellular bulk phase of the endometrial cells were negative with respect to the luminal fluid bulk phase. Unfortunately, Clemetson et al. confused these negative, transluminal membrane p.d. with a net negative charge on the surface of the luminal membrane of the endometrial cells. The surface charges can be expressed as a 'zeta potential', the value of which decays rapidly within a few Angstroms in a direction normal to the charged surface. The charges that give rise to zeta potential are those that cause electrostatic repulsion or attraction. While such charges may well exist on the surface of the luminal endometrial membranes (as they appear to exist on practically all cell surfaces) they are related only to the charged, dissociated iono-IO END 58