The evolution of stress response and fertility are considered important aspects driving the fitness of a species [1, 2], which are associated with the central nervous system through the hypothalamic-pituitary-adrenal (HPA) axis and hypothalamic-pituitary-gonadal (HPG) axis, respectively [3, 4]. And a cross talk between HPA and HPG is found [5], stress exerting an influence on fertility, causing fertility reduction and fitness loss threatening species persistence while the end products of HPG helping tune HPA axis-derived stress hormones [2, 5, 6]. Peripherally, many studies demonstrate that reproductive organs/tissues also play an important role in both the fertility and stress via corticotropin-releasing hormone (factor) family system (CRF system), the latter (stress) being precedingly described. In the peripheral reproductive system, CRF peptides (CRFp), including corticotropin-releasing hormone (CRH) and urocortins (UCNs, (UCN1–3)), emerge as critical factors in the process of fertilization and have attracted wide attention [7–10]. CRFp are observed to express similarly to the relevant receptors (CRFr, CRF1, and CRF2) in both the female and the male reproductive systems, functioning in an autocrine/paracrine way [11–13]. Moreover, CRF-binding protein (CRF-BP) is found to modulate CRFp levels participating in the process of reproductivity [14, 15]. Understanding the role of the CRF system in the reproductive system is beneficial for exploring therapeutic approaches of CRFp relevance, and indeed, the development of CRH knockout mice has been an important tool for addressing the physiologic and pathologic roles of CRH in fetal development and postnatal life [16]. This chapter will mainly focus on the distribution and role of CRFp in the peripheral reproductive organs.