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)

A case of diabetes insipidus is presented which appeared in a 13 year old girl associated with hormone-resistant amenorrhea; she went through two normal pregnancies and partutition at 22 and 25, indicating a fertile amenorrhea. During a total of 17 years of observation the amenorrhea persisted, with the exception of a few normal menstruation periods at the beginning of the disease. She remained permanently under treatment with pitressin tannate. Repeated administrations of estrogens, gestagens and chorionic gonadotrophin, had no effect. An endometrial biopsy revealed a presecretory phase. Acidophilic index in vaginal smears as well as serial determinations of urinary pregnanodiol indicated cyclic changes. Daily determinations of urinary pregnanodiol indicated cyclic changes. Daily determinations of plasma gonadotrophins during 28 days revealed normal levels, with normal FSH pulse and ovulatory type peak of LH. An LH-RH test gave marked and characteristic increase of both hormones. The data indicate the integrity of the hypothalamo-hypophyso-ovaric system, with cyclic changes and formation of corpus luteum, vaginal trophism and endometrial changes, concordant with the two normal pregnancies. In this case, the amenorrhea can only be explained by alteration of the usual endometrial vascular changes. The coexistence of diabetes insipidus and fertile amenorrhea is discused in relation with the possible participation of vasopressin in the mechanism of menstruation.
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PMID:[Fertile amenorrhea associated to diabetes insipidus]. 77 72

Twelve patients (10 women and 2 men) with a primary empty sella turcica were studied. Endocrine function tests were performed as follows: growth hormone (GH) was measured after insulin-induced-hypoglycaemia, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) after LH-releasing hormone, thyrotrophin (TSH) and prolactin after thyrotrophin-releasing hormone; pituitary reserve of adrenocorticotrophin (ACTH) was determined by measurement of plasma cortisol after lysine-vasopressin and 11 deoxycortisol after metyrapone. Five of the patients (group A) had no endocrine disturbance. Seven patients (group B) had a hypothalamo-pituitary disorder. Two of them had panhypopituitarism which appeared in one case after meningoencephalitis and in the other after a severe cranial trauma. In two cases an amenorrhoea-galactorrhoea syndrome with increased prolactin level (68 and 230 ng/ml) led to a diagnosis of a prolactin producing adenoma, which was confirmed by surgery. Finally three cases of amenorrhoeagalactorrhoea, with normal prolactin level, and/or diabetes insipidus remained unexplained. However, no causal relationship could be demonstrated between the pituitary disturbance and the "empty sella". Primary empty sella turcica is therefore a neuroanatomical and neuroradiological entity with no endocrine implication. A pituitary disorder might suggest a microadenoma or an incidentally associated disease.
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PMID:The primary empty sella an endocrine study on 12 cases. 98 92

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

A 33-year-old female presented in 1966 with striking pigmentation, typical of Addison's disease, and amenorrhea. Endocrine assessment then showed normal basal serum cortisol and urinary hydroxysteroid levels, but serum cortisol did not respond to stimulation with either exogenous ACTH or lysine vasopressin. Steroid replacement treatment was started. Treatment was discontinued by the patient on her own initiative and after some yr she was lost to follow-up. Reassessment in 1986 showed a pigmented patient who had continued in good health. She had a normal basal serum cortisol level with circadian variation. Plasma ACTH levels were high but showed diurnal rhythmicity and suppressed incompletely with 2 mg or 8 mg of dexamethasone/24 h. Plasma aldosterone levels were normal and showed appropriate postural changes, but plasma renin levels were high. This patient has an immunological profile of autoimmune disease with positive adrenal, thyroid microsomal and gastric parietal cell antibodies with a history of a premature menopause which may also be of autoimmune origin. She has been seen over a 20-yr period and despite her appearance still has no biochemical evidence of glucocorticoid or mineralocorticoid deficiency. It is suggested that the patient had compensated hypoadrenalism, with serum cortisol levels maintained in the normal range by high plasma ACTH levels and serum aldosterone levels maintained by high renin levels. The long term result of the high ACTH levels was increased skin pigmentation.
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PMID:Partially compensated hypoadrenalism presenting with persistent skin pigmentation. 254 90

Activation of the hypothalamus-pituitary-adrenal (HPA) axis is suggested to play a role in the stress-related inhibition of LH secretion. The aim of our study was to investigate the effects of vasopressin and oxytocin, which are increased in pituitary portal plasma in response to stress, and of glucocorticoids, the final product of HPA activation during stress, on basal plasma LH levels and on pituitary LH response to the GnRH test in amenorrheic (n = 33) and fertile (n = 13) women. Plasma LH levels were evaluated by radioimmunoassay in 2 different experimental conditions: 1. Basal secretion; 2. The GnRH test (10 micrograms + 10 micrograms after a 120-minute interval). These 2 evaluations were done in the presence of both placebo and a pharmacological dose of desmopressin (an analogue of vasopressin) (16.6 ngr/minute), oxytocin (0.2 ngr/minute) or hydrocortisone (4.1 mg/minute). None of these drugs modified basal plasma LH levels either in amenorrheic patients or in controls. Hydrocortisone inhibited the GnRH-induced LH increase in amenorrheic women. These data suggest that the glucocorticoids might play a role in LH secretion and indicate a possible participation of the HPA axis in the impairment of the hypothalamus-pituitary-gonadal axis in women with psychogenic amenorrhea.
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PMID:Glucocorticoids but not vasopressin or oxytocin inhibit luteinizing hormone secretion in patients with psychogenic amenorrhea. 272 8

In a 20-year-old woman, a complicated full-term delivery was followed by a 14-month history of galactorrhea, amenorrhea, and symptoms of hypocortisolism. Evaluation revealed the presence of an empty sella, hyperprolactinemia, and an isolated pituitary deficiency of ACTH, resulting in secondary adrenal insufficiency. The defect in ACTH secretion was apparently due to intrinsic pituitary rather than hypothalamic disease, because administration of lysine vasopressin did not stimulate ACTH release. An empty sella with hyperprolactinemia has been described before. However, to the authors' knowledge, isolated ACTH deficiency as a complication of postpartum hypopituitarism (atypical Sheehan's syndrome) in association with an empty sella and hyperprolactinemia has not previously been reported.
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PMID:Primary empty sella, hyperprolactinemia, and isolated ACTH deficiency after postpartum hemorrhage. 630 Dec 77

Opioid peptides are found throughout the central nervous system, and have profound effects on neuroendocrine function. In man, exogenous opiates and opioids elevate circulating prolactin, GH and TSH, and suppress the release of the gonadotrophins and pro-opiocortin-related peptides. However, unlike in other species, there is substantial evidence for a physiological role of endogenous opioids only in the case of the gonadotrophins and ACTH/LPH. Most evidence suggests that LH and FSH are modulated via the hypothalamus or amygdala, where concentrations of opioids and opioid receptors are very high. Endogenous opioids appear to be principally concerned with the frequency-modulated release of GnRH, and this may be important clinically in patients presenting with amenorrhoea. ACTH/LPH are under tonic inhibition by endogenous opioids acting at hypothalamic and/or pituitary levels, and changes in this inhibition may be responsible for the release of these peptides in response to certain forms of stress. It has been reported that the opiate antagonist, naloxone, is clinically useful in paradoxically inhibiting the release of ACTH in patients with Nelson's syndrome, but this requires adequate confirmation. Vasopressin is under biphasic opiate control, but the principal effect is probably opiate-mediated inhibition of vasopressin release. The endogenous ligand for this response is likely to be dynorphin. Suppression of vasopressin release by opiates may become a useful therapy in the treatment of the 'Syndrome of inappropriate ADH'.
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PMID:Brain opiates and neuroendocrine function. 632 67

A patient is described who developed diabetes insipidus during pregnancy. During a revised Carter test performed at 36 wk gestation using DDAVP (1-desamino-8-D-arginine-vasopressin), uterine activity was recorded with a maximum activity of 120 Montevideo Units. The induction of uterine activity by DDAVP in our patient might be related to the high endogenous oxytocin levels or to the far advanced state of amenorrhea. Post partum, the patient reported decreased vision, and the visual fields were found to be abnormal. A neurosurgical procedure followed, and the diagnosis of craniopharyngioma was made.
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PMID:Diabetes insipidus in pregnancy as a first sign of a craniopharyngioma. 718 32

Starvation-induced alterations of neuropeptide activity probably contribute to neuroendocrine dysfunctions in anorexia nervosa. For example, CRH alterations contribute to hypercortisolemia and NPY alterations may contribute to amenorrhea. Alterations of these peptides as well as opioids, vasopressin, and oxytocin activity could contribute to other characteristic psychophysiological disturbances, such as reduced feeding, in acutely ill anorexics. Such neuropeptide disturbances could contribute to the vicious cycle that has been hypothesized to occur in anorexia nervosa. That is, the consequences of malnutrition perpetuate pathological behavior.
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PMID:Neuropeptide abnormalities in anorexia nervosa. 873 16

Stress is a common cause of hypothalamic amenorrhoea. In our laboratory, we have studied the effects of an inflammatory-like stress on gonadotropin secretion and on the menstrual cycle in a nonhuman primate model. In this short review, we summarize some of our findings regarding the mechanisms whereby stress induces disturbances of reproductive function. Our data indicate that the hypothalamic-pituitary-adrenal axis, through the release of corticotropin-releasing hormone and vasopressin, plays a mediatory role. One type of action is exerted through a central process resulting in the inhibition of the gonadotropin-releasing hormone pulse generator. The other type is mediated by a peripheral pathway stimulatory to gonadotropin secretion. Activation of one or the other pathway is determined by the ovarian endocrine milieu. Both actions presumably result in deleterious effects on the menstrual cycle.
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PMID:Stress-related disturbances of the menstrual cycle. 924 Jun 27


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