Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased knowledge on the mechanisms whereby corticotropin releasing hormone (CRH) and opioid peptides mediate the effects of stress has helped us to understand the relationship between stress and disturbed reproductive function. Increases of CRH and beta-endorphin in the hypothalamus in stressful situations inhibits the secretion of gonadotropins, oxytocin and vasopressin. This may lead to amenorrhea, which often is a consequence of intensive training or psychological stress, or it may disrupt parturition and lactation. There is a relationship between ovarian function and opioid peptides in the hypothalamus. Opioid peptides increase during puberty and fall at the menopause. Oestradiol and progesterone increase beta-endorphin concentrations in the luteal phase of the menstrual cycle, and this is followed by a rapid fall at menstruation. These changes may mediate symptoms typical of the premenstrual syndrome. Rather intensive exercise is required to increase plasma concentrations of beta-endorphin and corticotropin. During labour the amounts of beta-endorphin and corticotropin reach the values found in athletes during maximal exercise. The placenta produces increasing amounts of CRH towards the end of pregnancy which may help the mother and fetus to withstand the increased demands of labour. The placenta may thus be involved in the adaptation of the stress mechanism during pregnancy. CRH has also a paracrine function in different biological processes of the placenta and fetal membranes. It is possible to counteract the deleterious effects of stress on reproductive function by the administration of opiate antagonists. Induction of ovulation with naltrexone has been shown in patients with hypothalamic amenorrhea but the effect on fertility is not known.
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PMID:Corticotropin-releasing hormone and opioid peptides in reproduction and stress. 175 18

PMS is probably a group of entities which include various symptoms that occur during the 7 to 10 days before menstruation and disappear a few hours after the onset of menstruation. The definition of PMS lacks objective criteria. The most common symptoms are irritability, bloating, aggressiveness, mastodynia, and headaches. The prevalence of PMS is estimated at 30 to 40 per cent. PMS is more prevalent among women working outside the home, alcoholics, women of high parity, and women with toxemic tendency; it probably runs in families. The etiology of PMS is no less obscure to us than when it was first described by Frank in 1931. No single theory has been established to explain the entire diversity of PMS symptomatology. The multitude of possible etiologic factors includes psychosocial bases, progesterone deficiency, prolactin excess, thyroid hypofunction, renin angiotensin alternations, antidiuretic hormone excess, decreased colloidosmotic pressure, endorphin activity alternations, serotonin metabolism alternations, prostaglandin action, vitamin deficiency, and such unconventional theories as the ovarian infection or the "yeast overgrowth" theory. A partial resolution of this divergence of hypotheses comes from the biopsychosocial model developed by Keye and Trunnel. According to this model, a biologic, perhaps genetically determined, predisposition to PMS is realized when past and present life experiences, attitudes, beliefs, coping styles, and social forces interact to stress a woman. The diagnosis of PMS is based on establishing a relationship between the luteal phase of the cycle and the symptoms. The evaluation of PMS patients includes the use of a monthly diary to scale the symptoms, a physical examination, and biochemical studies to rule out other disorders. Management includes education, reassurance, and drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The premenstrual syndrome. 218 58

The premenstrual syndrome (PMS) is a major clinical entity afflicting a large segment of the female population. Available information are descriptive in nature and the etiology of this syndrome remains unclear. In this review, both biochemical and psychosocial elements of the syndrome have been explored in an effort to redefine the pathophysiology of this seemingly multifactorial psychoneuroendocrine dysfunction. We propose that luteal phase sensitivity to and subsequent withdrawal from the central effects of the neuropeptides beta-endorphin and alpha-melanocyte-stimulating hormone result in a cascade of neuroendocrine changes within the brain-hypothalamus-pituitary complex. Modulation of neurotransmitter function by these peptides may produce alterations in mood and behavior as well as enhance pituitary release of prolactin and vasopressin. Variable gonadal steroid modulation of these responses from subject to subject likely accounts for the heterogeneous clinical manifestations of the PMS.
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PMID:Premenstrual syndrome. 700