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)

In adipocytes that have been deprived of growth hormone (GH) for at least 3 hr, GH elicits a transient insulin-like response that is followed by a period of refractoriness to further insulin-like stimulation. Exposure of adipocytes to GH in the first hour of a 3-hr incubation prevents the appearance of insulin-like sensitivity. Intracellular Ca2+ concentration [( Ca2+]i) was measured in individual adipocytes that were loaded with fura-2 hexakis(acetoxymethyl) ester after preincubation in the presence (refractory) or absence (sensitive) of recombinant human GH at 100 ng/ml. Using a dual nitrogen laser imaging microscope with computer-assisted image processing to measure fluorescence changes, we observed that resting [Ca2+]i was 220 +/- 10 nM in refractory adipocytes and 110 +/- 6 nM in sensitive adipocytes (P less than 0.001). GH had no acute effect on [Ca2+]i in sensitive adipocytes but caused a sustained 3-fold increase in [Ca2+]i in refractory cells within 3 min (P less than 0.001). Insulin did not change [Ca2+]i in either sensitive or refractory adipocytes. In refractory cells treated with insulin and GH simultaneously, insulin completely blocked the rise in [Ca2+]i due to GH. Oxytocin elicited a prompt increase in [Ca2+]i followed by a quick return to resting levels in both sensitive and refractory cells. These findings indicate that basal [Ca2+]i is increased in refractory cells and that GH produces a sustained rise in [Ca2+]i only in refractory adipocytes. We suggest that the sustained increase in [Ca2+]i produced by GH in refractory cells prevents the expression of the insulin-like response.
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PMID:Refractoriness to growth hormone is associated with increased intracellular calcium in rat adipocytes. 186 2

Data are presented to show that vasoactive intestinal peptide (VIP) is synthesized and secreted by the hypothalamus and anterior pituitary and that it participates in the regulation of pituitary functions. Immunoreactive VIP in the hypothalamus and pituitary is increased following estrogen treatment and adrenalectomy and is reduced in hyperprolactinemic states. The level of VIP mRNA in the hypothalamus is increased during lactation and sexual maturation, while that in the anterior pituitary shows a sexual dimorphism and is increased with estrogen treatment and hypothyroidism. All these findings suggest a physiological regulation of hypothalamic and pituitary VIP gene expression in relation to its potential role as a neuroendocrine hormone. Furthermore, VIP stimulates prolactin (PRL) release at concentrations attainable in the hypophyseal-portal blood. Passive immunoneutralization studies with anti-VIP antisera suggest that endogenous VIP acts at multiple loci in the hypothalamic-pituitary axis to regulate PRL secretion, interacting possibly with other regulators of PRL secretion such as estrogen, serotonin, cholecystokinin, prostaglandins, galanin and oxytocin. Regarding other pituitary functions, although VIP has been shown to release growth hormone, ACTH, and vasopressin in vivo and in vitro, the physiological significance of these findings remains to be determined.
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PMID:Vasoactive intestinal peptide in the hypothalamus and pituitary. 190 91

Changes in the structure and function of five neuropeptide families during evolution are considered. The families of gonadotropin-releasing hormone (GnRH), corticotropin-releasing factor (CRF), growth hormone-releasing hormone (GH-RH), somatostatin (SS), and vasopressin/oxytocin (VP/Oxy) are used as models to illustrate the importance of a phylogenetic approach in understanding neuropeptide structure/activity relationships, precursors, processing, gene duplication, novel locations and functions, and gene-associated peptides.
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PMID:Neuropeptide families: an evolutionary perspective. 197 5

The responses of the adenohypophyseal hormones adrenocorticotrophin (ACTH), growth hormone (GH), thyroid stimulating hormone (TSH), prolactin, luteinizing hormone (LH) and follicle stimulating hormone (FSH) to sub-maximal doses of hypothalamic releasing factors were studied in six lean male volunteers (age 23-35 years) with and without infusions of oxytocin (OXT). OXT infusion (mean plasma concentration 133.6 +/- 2.6 pmol/l) completely inhibited the plasma ACTH responses to corticotrophin releasing hormone (CRH) (saline, peak increment ACTH 1.61 +/- 0.75 pmol/l; OXT, peak increment ACTH - 0.04 +/- 0.28 pmol/l; P less than 0.05). OXT infusion had no significant effect on the GH response to growth hormone releasing hormone (GHRH), the TSH and prolactin responses to thyrotrophin releasing hormone (thyroliberin, TRH) or the LH and FSH responses to gonadotrophin releasing hormone (luteoliberin, GnRH). The data support a role for OXT in the modulation of ACTH secretion in man.
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PMID:The effect of oxytocin infusion on adenohypophyseal function in man. 216 Aug 73

Human thymic epithelial cells (TEC) were grown in culture and confirmed to be keratin positive (98-100%) and epidermal growth factor (EGF) responsive. Bovine pituitary extracts (BPE) stimulated the proliferation of TEC. The proliferation of TEC was confirmed by cell counts and radioautography. The BPE was active as measured by tritiated thymidine incorporation in the absence of serum and in the absence of EGF. Individual anterior pituitary hormones (growth hormone, prolactin, ACTH, FSH, LH, TSH) and posterior pituitary hormones (vasopressin and oxytocin) were inactive alone to stimulate TEC proliferation. The effect of EGF but not BPE was blocked by an antibody to EGF suggesting that the active component of BPE is not EGF. Purification of the factor is in progress. The observations suggest that this pituitary-derived factor(s) may regulate thymic function in vivo.
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PMID:A pituitary factor induces thymic epithelial cell proliferation in vitro. 247 91

A review of current advances in anatomy, physiology and pharmacology of vasoactive intestinal polypeptide (VIP) is presented. VIP is a basic 28-aminoacid peptide of molecular weight 3300. Nerves immunoreactive to VIP are in the heart, lung, digestive and genitourinary tract, eye, skin, ovaries and thyroid gland. In the central nervous system VIP-ergic neurons are found primarily in telencephalic areas. Here, VIP provokes the excitation, vasodilatation and together with noradrenaline participates in the regulation of cortical energy metabolism. VIP-ergic neurons are mainly present in afferent pathways of the spinal cord with higher density in the sacral segments. Anatomic distribution of VIP-ergic neurons suggests involvement in pain transmission and integration of the sacral autonomic reflex pathways. The biologic effects of VIP in periphery are the vasodilatation, relaxation of smooth muscle and influence on exocrine glands secretion. In the endocrine system VIP stimulates the secretion of different hormones (prolaction, growth hormone, oxytocin, vasopressin, ovarial and thyroid hormones). VIP-ergic innervation is changed in some organs during the diseases of those organs. Practical exploatation of this knowledge is limited at present because effective, non-polypeptide agonists and antagonists are not available yet.
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PMID:[Vasoactive intestinal polypeptide: a potential neurotransmitter]. 257 79

The responses of plasma adrenocorticotrophin (ACTH), cortisol, growth hormone (GH) and prolactin to insulin-induced hypoglycaemia were studied in six lean male subjects (age 22-29 years). Intravenous insulin tests were performed with and without oxytocin infusion. Blood sugar nadir occurred at the onset of symptoms (time S) with no significant differences between oxytocin and saline infusion. During the oxytocin infusion mean plasma oxytocin increased from 1.9 pmol/l to 138 pmol/l. Peak increase in plasma ACTH (oxytocin 266 +/- 54 ng/l; saline 281 +/- 43 ng/l, mean +/- SEM) was at S + 10 min while peak plasma cortisol (oxytocin 680 +/- 47 nmol/l: saline 656 +/- 40 nmol/l) was measured at S +/- 60 min, peak GH (oxytocin 96 +/- 17.8 mU/l; saline 106 +/- 18.6 mU/l) at S + 60 min and prolactin (oxytocin 1332 +/- 239 mU/l; saline 1242 +/- 273 mU/l) at S + 30 min. There were no significant differences in plasma concentrations of ACTH, cortisol, GH or prolactin between saline and oxytocin infusion. The results indicate that oxytocin has no effect on plasma ACTH, cortisol, GH and prolactin responses to insulin-induced hypoglycaemia. In particular they fail to support previous studies which suggested an inhibitory role for oxytocin in ACTH secretion.
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PMID:The effect of oxytocin infusion on adenohypophysial and adrenal cortical responses to insulin-induced hypoglycaemia. 285 20

Plasma concentrations of oestrogen-stimulated neurophysin (ESN), prolactin, and growth hormone were measured before and after the first treatment in a course of electroconvulsive therapy (ECT) given to 25 psychiatric patients and during induction of anaesthesia in 9 women undergoing elective cholecystectomy. Prolactin levels rose and growth hormone levels fell during both cholecystectomy and ECT, but ESN levels rose only after ECT. The peak ESN response to ECT was significantly greater (p less than 0.005) in the 16 depressed patients who recovered than in the 9 who did not. All patients in whom plasma ESN concentration increased by more than 100% satisfactorily recovered from their depressive illness. If a 63% increase in ESN concentration is used to classify all subjects, 12% are misclassified by outcome at 2 months. The extent of the ESN response, but not the prolactin or growth hormone responses, correlated with improvement in symptoms measured by Hamilton Rating Scale for Depression and the Montgomery and Asberg Depression Rating Scale.
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PMID:Oestrogen-stimulated neurophysin and outcome after electroconvulsive therapy. 287 18

This consideration of the influence of endogenous opioid peptide systems on GnRH and oxytocin neurones serves to illustrate some of their possible regulatory interactions with other neuroendocrine systems. Opioids are known to influence the secretion of all the anterior pituitary hormones (see Grossman & Rees, 1983) and these effects are likely to be mediated, at least in part, in the hypothalamus. For example, inhibitory effects of opioids have also been described on secretion from the median eminence of somatostatin (Drouva et al. 1981b) and dopamine (Wilkes & Yen, 1980), and this site of action probably accounts for at least some of the stimulatory effects of exogenous opioids on plasma growth hormone and prolactin levels respectively. For the GnRH neurones the influence of endogenous opioid neurones, possibly the arcuate beta-endorphin system, appears to be mediated indirectly by inhibiting release of excitatory or facilitatory monoamines. This opioid-adrenergic interaction itself appears to be central in the regulation of gonadotrophin secretion and mediation of the feedback effects of gonadal steroids in the brain. The steroids may act directly on both adrenergic and opioid neurones, altering monoamine metabolism and release which may, in turn, regulate numbers of adrenergic receptors perhaps located on the GnRH neurones. Opioid peptide levels are also modulated by steroids probably reflecting altered synthesis and/or processing of precursors. Regulation of the opioid-adrenergic input may not only acutely affect the secretory output of the GnRH neurones but also influence synthesis or processing of GnRH itself (see Kalra & Kalra, 1984) and its degradation by hypothalamic peptidases (Advis, Krause & McKelvy, 1983). Oxytocin neurones demonstrate three further levels of interaction with endogenous opioid peptides. First the anatomical organization of the oxytocin neurones has enabled a clear demonstration of the action of opioids close to the secretory terminals to uncouple the generation of electrical activity from release of peptide. Secondly, both the oxytocin and the neighbouring vasopressin neurones themselves synthesize, process and package opioid peptides. These neurones thus provide a clear example of co-existence of several biologically active products in individual neurones. The relative expression of the different gene products may prove to be a further level of control of opioid influences on the oxytocin and vasopressin neurones.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Endogenous opioid peptides and hypothalamic neuroendocrine neurones. 299 85

Extracellular action potentials were recorded from 48 single units located in the hypothalamic arcuate and ventromedial nuclei. Fifteen percent of the cells were identified as projecting to the median eminence and some of these cells may have belonged to the tuberoinfundibular dopaminergic systems. Responses of all cells to stimulation of the ipsilateral supraoptic nucleus were recorded; 17% of ventromedial nucleus neurons were antidromically identified as projecting to the supraoptic nucleus. None of the latter cells was also identified as projecting to the median eminence. Three of six identified tuberoinfundibular and eight unidentified ventromedial nucleus cells were found to be excited by stimulation of the supraoptic nucleus. One arcuate cell identified as projecting to the median eminence was nonresponsive to supraoptic stimulation. Orthodromic inhibitory responses were recorded from 17% of all cells recorded but no inhibitory responses were recorded from cells identified as projecting to the median eminence. We suggest that these results may provide some neurophysiologic explanations for the observed interrelationships between oxytocin and prolactin secretion, and between vasopressin and growth hormone secretion.
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PMID:Electrophysiologic evidence for connections between the supraoptic and the arcuate/ventromedial hypothalamic nuclei in the rat. 301 86


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