The human tachykinin, endokinin (EK), is processed into a 41mer in the human placenta. As synthetic EK(1041) is as potent as substance P at the NK1R, it is likely that the primary function of EK is as the principal placental NK1R agonist mediating local beneficial vasodilatation. Although the emetic and sialogogic actions of substance P are well known, its complete absence from the placenta probably explains why its role in pregnancy has not been studied. I propose that the potent natural placental NK1R agonist, EK, by spilling in to the mothers circulation, should now be recognised as the likely cause of emesis and sialorrhea in pregnant women. As EK is post-translationally modified specifically in the placenta with a phosphocholine (PC) moiety, it would bind to placental C-reactive protein (CRP) and form a pentameric agonist complex resulting in local NK1R aggregation/activation. Circulating PC-free EK released from peripheral tissues (e.g. from the lungs during smoking), on occupying placental/uterine NK1Rs, could reduce the receptor aggregation induced by placental pentameric PC-EK/CRP, and may account for the poor placentation/vascularisation seen in smokers. The release of EK from lung tissue may also explain the lower incidence of emesis in pregnant smokers by down regulation of the associated NK1Rs in the area postrema of the medulla oblongata.