Pathogenesis of the crosstalk between reproductive function and stress in animals—part 1: Hypothalamo–pituitary–adrenal axis, sympatho‐adrenomedullary system and kisspeptin

Abstract

AbstractStress is defined as a disruption of the body homeostasis in response to modest as well as perceived challenge. Two main physiological routes, the hypothalamic–pituitary–adrenal system (HPA) and the sympatho‐adrenomedullary system (SAM), aim to maintain or restore homeostasis by mutual interaction. SAM is quickly‐reacting as it primarily works through the nervous system—the sympathetic nervous system. In response to stress, signals are sent to activate the adrenal medulla which releases catecholamines (primarily adrenaline and norepinephrine). The catecholamines have a momentary effect on the body's organs that are prepared for a fight situation. At the same time, the stressor activates the HPA axis by signals from the brain causing secretion of the pituitary hormone adrenocorticotropic hormone (ACTH). ACTH acts on the adrenal cortex, which secretes glucocorticoids, including cortisol. Since HPA primarily works through hormones, the system is slightly slower than SAM and gives rise to a metabolic effect. While short‐term stress response is an adaptive and beneficial process, chronic or excessive stress can lead to a range of negative health outcomes including reproductive disorders and infertility. Several mechanisms have been proposed to explain the link between stress and reproduction. This includes in particular kisspeptin, which is closely related to reproduction, as it is a powerful stimulator of the Hypothalamic–pituitary–gonadal (HPG) system. The present review, through current knowledge in various male and female species, deals with the role of the SAM and the HPA, including the major action of kisspeptin and glucocorticoids that trigger the consequences of psychological or physiological stress on reproductive function.