In this paper we analyse three general models of sexual selection. In one of the models, an ordered series of multiple alleles determines a series of distinct phenotypes in a dominance hierarchy, each phenotype being dominant to all phenotypes below it in the hierarchy. In another model, some alleles determine an ordered hierarchy of dominant phenotypes; others are co-dominant, each genotype producing a separate phenotype except when in combination with one of the dominant alleles. In the third model, two groups of alleles form two separate dominance hierarchies with co-dominance between alleles from each group. In the model with ordered dominance, a unique, globally stable equilibrium is attained at which the frequencies of the phenotypes are exactly proportional to their rates of preferential mating. In the model with dominance and co-dominance, a unique, globally stable equilibrium is also attained. The gene frequencies at equilibrium are given by hybrid expressions combining the frequencies for complete dominance with those for complete co-dominance. An explicit solution is not found when the alleles form two separate dominance hierarchies; but a unique, globally stable equilibrium exists from which the equilibrium frequencies can be obtained by an iterative method. We also analyse some special models with a limited number of alleles and different dominance and co-dominance relationships. In a model with inclusion relationships between the alleles, an allele giving rise to one sexually selected dominant phenotype may also be included with another allele to give rise to a separate sexually selected phenotype. Thus the genotypes A1A1, A1A2 and A1A3, may represent one sexually selected phenotype; the genotypes A1A1, A11A2, A1A3, A2A2 and A2A3, may represent another sexually selected phenotype. This is a model of how sexual selection might operate in favour of increasing expression of a character: some females may respond to males with either the alleles A1 or A2; other females may only respond to males with the more extreme phenotype determined by the allele A1. At equilibrium, the allele A2 will have been eliminated.