Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine whether normal morphological development occurs in pituitary corticotrophs deprived of products of the hypothalamic paraventricular nucleus (PVN), e.g. corticotropin releasing hormone and arginine vasopressin (AVP), after PVN lesions. In addition, we have attempted to ascertain if the neurophysin/AVP-positive fibers innervating the fetal sheep anterior pituitary are affected by PVN lesions. The experimental groups consisted of fetal sheep in which 1) hypothalamic PVN lesions were placed at 118-122 days gestation (dGA) and the fetuses subsequently harvested while still in utero at 157 dGA or more (PVNX; n = 5); 2) sham PVN lesions were placed at 118-122 dGA and subsequently harvested as newborn lambs immediately after birth at 146.5 +/- 0.9 (mean +/- SEM) dGA combined with two uninstrumented fetuses harvested at 144 dGA or more but not in labor (perinatal; n = 6); and 3) no instrumentation was placed, and the fetuses were harvested at 120 dGA (control; n = 4). Two ACTH-immunoreactive cell types were seen in the anterior pituitary: 1) fetal cells: large and variably stained, often columnar, occurring in clusters and arranged in palisades; and 2) adult cells: smaller, darkly staining, and angular, occurring singly or in small groups. Quantification of the distribution of the two ACTH cell types was performed by scanning sections from a one in six series from each pituitary and estimating the percent area of each section in the well that showed adult type staining only. The observer was blind to the treatment group assignment of the sections. The estimated percentages of the portion of the pituitaries of each group that contained adult-type cells only were as follows: PVNX, 42.8 +/- 10.0%; perinatal, 90.9 +/- 2.1%; and control, 3.7 +/- 1.1% (mean +/- SEM; P less than 0.05 for all comparisons). There were no qualitative differences between all groups in the appearance of neurophysin-positive fibers innervating the anterior pituitary. AVP staining was strong in the internal zone of the median eminence in all groups, but was absent in the external zone of PVNX fetuses only. The intermediate pituitary lobes stained darkly in all groups. We conclude that lesions of the PVN at 120 dGA delay development of fetal pituitary corticotrophs, but have no effect on the presence of neurophysin-positive nerve fibers in the anterior pituitary.
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PMID:Hypothalamic paraventricular nuclear lesions delay corticotroph maturation in the fetal sheep anterior pituitary. 132 50

Cerebrospinal fluid hormones, monoaminergic metabolites, and dynorphin A (1-8 sequence) were examined in 43 children with severe, primary obsessive-compulsive disorder. Cerebrospinal fluid levels of 5-hydroxyindoleacetic acid were positively correlated with one of eight obsessive-compulsive disorder severity ratings and three of seven measures of improvement following 5 weeks of treatment with clomipramine hydrochloride. Arginine vasopressin concentration was significantly and negatively correlated with several ratings of obsessive-compulsive disorder symptom severity, while oxytocin concentration was positively correlated with depressive symptoms. The ratio of arginine vasopressin to oxytocin was also negatively correlated with obsessive-compulsive disorder and depressive symptoms. Comorbid affective disorder was associated with decreased arginine vasopressin concentrations, while concomitant anxiety disorder was associated with increased oxytocin. Dynorphin A (1-8 sequence), homovanillic acid, corticotropin, 3-methoxy-4-hydroxyphenylglycol, and corticotropin releasing hormone were not significantly related to obsessive-compulsive disorder symptoms. These results seem to indicate that arginine vasopressin may be related to obsessive-compulsive disorder symptom severity, while 5-hydroxyindoleacetic acid might be associated with drug response.
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PMID:Cerebrospinal fluid neurochemistry in children and adolescents with obsessive-compulsive disorder. 137 Jan 97

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

We have recently demonstrated that corticotropin releasing hormone (CRH) potentiates the contractile response to oxytocin of human gestational myometrium, using a high flow microsuperfusion system and electrical field stimulation. We now report this potentiation to be equivalent to that of 1 nM prostaglandin F2 alpha (PGF2 alpha), while 10 nM PGF2 alpha did not potentiate the response to oxytocin. Prostaglandin E2 (PGE2) also showed no augmentation of the contraction force of the myometrium in response to oxytocin. The CRH potentiated response was inhibited by the lipoxygenase and cyclooxygenase inhibitor BW755C (1 microM) and by indomethacin (0.1 microM), but not by the lipoxygenase inhibitor BW4C (1 microM). Measurements of prostaglandins in the superfusate showed no significant trends. It is concluded that the potentiation of contraction force to oxytocin by CRH is dependent on prostaglandins, probably PGF2 alpha and that leukotrienes, generated via the lipoxygenase pathway are not involved.
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PMID:Role of prostaglandins and leukotrienes in the synergistic effect of oxytocin and corticotropin-releasing hormone (CRH) on the contraction force in human gestational myometrium. 177 36

The opioid peptide, beta-endorphin, originates from proopiomelanocortin (POMC) under the influence of corticotropin releasing hormone (CHR). It increases the threshold of pain and has a certain influence on the formation of hypophyseal hormones, especially in stress. It is found that beta-endorphin stimulates the secretion of prolactin, a growth hormone, and vasopressin; it inhibates formation of follicle-stimulating and luteinizating hormones, oxytocin and dopamine, and gonadotropin, a releasing hormone. The process of acetylization decreases its activity. The results of experimental trials revealed that acetylisation in the foetal period was absent. The aim of the study was to define beta-endorphin concentration during normal vaginal labor and Cesarean section. Samples of peripheral blood of patients with spontaneous vaginal labor (n = 15) and of those in whom labor was operatively terminated (Cesarean section) (n = 10), were analysed. Values of this opiate were determined in the umbilical cord of newborn infants, in the amniotic fluid and placental compartment. The obtained results were statistically analysed. In intrapartum beta-endorphins were significantly increased reaching the highest level during expulsion (326 pg/ml); in the placental compartment these values were higher (in retroplacental blood 514 pg/ml) reaching the highest value of 917 pg/ml, p less than 0.01 in the placenta. In Cesarean section beta-endorphin values in the peripheral blood showed no significant differences during spontaneous vaginal labor. However, increased values of this natural opiate were observed six hours after surgery. Beta-endorphin concentrations in the placental compartment and the placenta during normal vaginal labor were significantly higher in comparison with labor by Cesarean section (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The opioid peptide, beta-endorphin, in spontaneous vaginal delivery and cesarean section]. 180 97

In the adult male Wistar rat a 2-fold 2-min restraint stress exposure, repeated 15 min apart, activated the adrenocortical secretion more than a single one would have. However, in rats with a pharmacological block of the endogenous CRF release, exogenous CRH (0.3 micrograms/kg iv), administered 15 min after a first similar dose, was unable to stimulate pituitary-adrenocortical activity above the level attained with the first peptide injection. On the contrary, in the same conditions exogenous arginine vasopressin (AVP) (0.3 micrograms/kg iv) administered 15 min after CRH, was able to further stimulate pituitary-adrenocortical activity. Using the same experimental procedure, oxytocin (0.3 micrograms/kg iv) was found to be totally inactive. The physiological import of these findings was investigated in the Brattleboro rat, genetically lacking in endogenous AVP, in which, unlike the control Long-Evans strain, the 2-fold stress exposure did not cause an increase in plasma corticosterone concentration greater than that of a single exposure. These results suggest that endogenous AVP is essential in sustaining adrenocortical activation in circumstances in which pituitary refractoriness towards CRH stimulation intervenes.
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PMID:Evidence for a specific role of vasopressin in sustaining pituitary-adrenocortical stress response in the rat. 203 82

The neurotransmitter histamine participates in the neuroendocrine regulation of pituitary hormone secretion by an indirect action at a hypothalamic level where histaminergic neurons are abundant. The effect of histamine is caused by activation of postsynaptic H1- or H2-receptors. Histamine stimulates the secretion of ACTH, beta-endorphin (mediated by CRH and AVP), alpha-MSH (mediated by dopamine and peripheral catecholamines), and PRL (mediated by dopamine, serotonin and AVP), and participates in the stress-induced release of these hormones and possibly in the suckling- and estrogen-induced PRL release. The release of GH and TSH is predominantly inhibited by histamine; however, uncertainty exists regarding its role and the hypothalamic factors involved. Histamine increases the secretion of LH in females (mediated by GnRH), and may be involved in the mediation of the estrogen-induced LH surge. AVP and oxytocin are stimulated by histamine, probably by an effect in the supraoptic and paraventricular nuclei of the hypothalamus.
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PMID:The role of histamine in the neuroendocrine regulation of pituitary hormone secretion. 206 91

Cold exposure increases blood levels of TSH and thyroid hormones by stimulating the secretion of TRH from the median eminence. Thyroid hormones reduce TRH release and cellular levels of TRH mRNA. Using quantitative in situ hybridization to measure changes in cellular levels of various neuropeptide mRNAs, the present studies demonstrate that cold exposure also increases cellular levels of TRH mRNA in neurons of the paraventricular nucleus (PVN), supporting the concept that TRH mRNA levels are reflective of TRH secretion in these neurons. The effect of cold appeared to be specific for TRH expression in the PVN, because cold exposure did not influence cellular levels of TRH in the reticular thalamic nucleus or beta-actin and oxytocin mRNAs in the PVN. Cellular levels of mRNA encoding CRH were elevated by cold exposure. This latter observation is predictable based on the cold-induced activation of the hypothalamic-pituitary-adrenal axis. There was a 24-h rhythm and a time of day difference in the effect of cold on TRH mRNA levels in the PVN. Time of day differences in the effect of cold on CRH mRNA levels were not apparent. Cold exposure appeared to elevate TRH mRNA levels in all neurons of the PVN, indicating that the neurally mediated effect of cold on TRH expression can override the inhibitory effects of circulating T3 within the same neuronal population.
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PMID:Cold exposure elevates cellular levels of messenger ribonucleic acid encoding thyrotropin-releasing hormone in paraventricular nucleus despite elevated levels of thyroid hormones. 212 45

This experiment was designed to test further the hypothesis that vasopressin is the major mediator of the ACTH response to activation of central alpha 1-adrenoceptors in the rat. The alpha 1-adrenergic agonist methoxamine was given intracerebro-ventricularly to conscious vasopressin-deficient (homozygous Brattleboro) and normal rats bearing venous and intracerebro-ventricular cannulae. Methoxamine stimulated the secretion of ACTH in the normal, but not in the vasopressin-deficient, rats. The data confirm that vasopressin, rather than CRH-41 or oxytocin, is the major hypothalamic peptide that mediates the effects of central alpha 1-adrenoceptors on the pituitary corticotrophs.
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PMID:Brattleboro rats have deficient adrenocorticotropin responses to activation of central alpha 1-adrenoceptors. 217 37

Previous studies have suggested the subfornical organ (SFO) to be the CNS site at which circulating angiotensin (ANG) acts to influence a variety of regulatory control mechanisms. We have utilised electrophysiological techniques: 1. to examine the neural connections through which the SFO exerts such control over hypothalamic regulatory control centres; 2. to investigate the responsiveness of neurons in a second circumventricular organ, the area postrema (AP), to circulating peptides. In accordance with previous endocrine studies we have demonstrated excitatory influences of SFO efferents on hypothalamic neurosecretory neurons putatively identified as vasopressin, oxytocin, CRH, and LHRH secreting. In addition systemic ANG increased the activity of the former three groups of these neurons, an effect which was abolished by destruction of the SFO. Single unit recordings from AP neurons have demonstrated subpopulations of cells in this regions to be sensitive to either circulating ANG or changes in blood pressure.
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PMID:Circumventricular structures: CNS sensors of circulating peptides and autonomic control centres. 236 60


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