Stress Effects on the Excretory and Reproductive Systems
The reproductive system is responsible for the propagation of species, which is equally affected by both internal and external conditions. The hypothalamic-pituitary-adrenal (HPA) axis is the regulatory axis of the reproductive system. It is regulated by corticotropin-releasing hormone (CRH) and arginine-vasopressin (AVP). Besides, gonadotropin-releasing hormone (GnRH) is the major regulatory hormone for the hypothalamic–pituitary–gonadal (HPG) axis. Besides, the latter is affected by stress (Love, Chin, Wynne‐Edwards, & Williams, 2005). The paper seeks to show how the hormonal response to stress affects the human reproductive function.
Stress activates the hypothalamic-pituitary-adrenal (HPA) axis, which controls the female reproductive system in various ways. It inhibits the work of the latter (Sanders, 2009). One of the crucial hormones that control the HPA axis is corticotropin-releasing hormone (CRH). It is responsible for inhibiting the secretion of hypothalamic GnRH. Besides, it also affects the production of pituitary luteinizing hormone (LH). In addition, it influences the process of progesterone and ovarian estrogen secretion. It leads to the abnormal absence of menstruation, a condition known as the “hypothalamic” amenorrhea of stress. Some effects that lead to the latter include chronic excessive exercise, malnutrition, depression and anxiety. The second hormone affecting the female reproductive function through the HPA axis is arginine-vasopressin (AVP). It stimulates the secretion of adrenocorticotropic hormone (ACTH) (Kalantaridou, et al., 2010). AVP also has a grea influence the brain to control the sexual behavior of the female individual (Veenema & Neumann, 2008).
CRH and AVP hormones regulation of the HPA axis has a profound impact on human reproduction. Stress acts as a trigger for these hormones. Consequently, their secretion affects the reproduction function of the individual. The response to CRH in the female reproductive system takes place in several organs. These include the ovaries, as well as placental trophoblast, decidualized endometrial stroma, and endometrial glands (Kalantaridou, Makrigiannakis, Zoumakis, & Chrousos, 2004). Ovarian CRH has several effects. Its high secretion causes the premature ovarian failure. On the other hand, the lack of the secretion of ovarian CRH leads to anovulation, which is the failed release of ova for periods longer than three months. Other effects of the low secretion of ovarian CRH include the corpus luteum and ovarian dysfunction (Kalantaridou et al., 2004). On the other hand, the under-secretion of uterine CRH can lead to infertility. Another possible effect is the incidence of the recurrent spontaneous abortion. Finally, there is placental CRH, the over-secretion of which may lead to premature labor (Kalantaridou et al., 2004). It can cause preeclampsia portrayed by hypertension and protein in the urine and eclampsia characterized by seizures. Incidences of the under-secretion of placental CRH may lead to delayed labor. The hormonal signal regulates reproduction by inhibiting the reproductive activity until overcoming a stressful condition. Such inhibition is an evolutionary mechanism to conserve ressources (Reeder & Kramer, 2005).
The physiological effects of the dysregulation of ovarian CRH include the suppression of female sex and ovulation. The influence of glucocorticoids on the ovary, uterus, and placenta is directly linked with gametogenesis. Besides, it inhibits the production and discharge of follicle stimulating hormone (FSH) and luteinizing hormone (LH), affecting the gonadal function in the female reproductive system. Glucocorticoids also affect the release of gonadotropin-releasing hormone (GnRH), which varies with the menstrual cycle and affects follicular growth. Decidualization is a physiological effect associated with uterine CRH and early maternal tolerance (Kalantaridou et al., 2004). Placental CRH physiologically affects the term of pregnancy by causing premature labor (Kalantaridou et al., 2004). Psychologically, the hormones are associated with depression during pregnancy and the control of arousal. Hypercortisolism leads to the suppression of adrenaline and depressive periods during pregnancy. Moreover, it is associated with an increase in autoimmunity in the latter half of the pregnancy (Kalantaridou et al., 2004). Glucocorticoid stress hormones suppress GnRH boosting the GnIH suppressor (Sanders, 2009). Stress is associated with the release of stress hormones, which inhibit reproductive hormones.
In conclusion, CRH and AVP hormones regulating the HPA axis have a profound impact on the human reproduction process. Stress acts as a trigger for these hormones. Consequently, the secretion of the hormones affects the reproductive function of the individual.