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)

Several peptide hormones are effective when administered intranasally (in); these include oxytocin, vasopressin, insulin, glucagon, and calcitonin. With regard to GHRH and CRH, previous studies demonstrated that their bioavailability following in administration was very low. In this study we evaluated the serum GH response to 50 micrograms GHRH iv and to 700 micrograms GHRH in, the latter given alone and with 5 and 15 mg sodium-glycocholate (SGC), a surfactant, in six normal men. The bioavailability of in GHRH, calculated as net GH secretory area, was very low, and increased to 7% that of iv GHRH when SGC was used. In the same men, 50 micrograms CRH was administered both iv and in, alone and with 5 and 15 mg SGC. The bioavailability of in CRH, calculated as net cortisol secretory area, was very low and increased to 100% that of iv CRH when 15 mg SGC was used. These data indicate that the efficacy of GHRH and CRH administered in is significantly augmented by SGC.
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PMID:Effect of intranasal growth hormone-releasing hormone and corticotropin-releasing hormone administration on growth hormone and cortisol release: improved bioavailability by means of sodium-glycocholate. 249 80

Ether and restraint stress-induced peripheral plasma corticotropin releasing hormone (CRH), arginine vasopressin (AVP), oxytocin (OXY) and adrenocorticotropin (ACTH) levels were measured by radioimmunoassays. Plasma CRH, AVP, OXY and ACTH rose to approximately twice the level of control rats 2 min after the onset of a 1-min exposure to ether. Plasma CRH rose further 5 min after the onset of ether stress, while plasma AVP and OXY returned to the baseline levels at 5 min. Plasma CRH, OXY and ACTH showed significant elevation 2 min after the onset of restraint stress, while plasma AVP did not show a significant change. Plasma OXY and ACTH rose further 5 min after the onset of restraint stress, whereas plasma CRH returned to baseline levels. CRH and OXY concentrations in the hypothalamic median eminence decreased 5 min after the onset of ether exposure and restraint, while the AVP concentration did not differ from control levels. The results, including the discrepancy between plasma CRH and ACTH 5 min after stress, suggest that CRH in the peripheral plasma is derived from both hypothalamic and extrahypothalamic tissues. The levels of stress-induced CRH in the peripheral plasma were sufficient to stimulate ACTH release. These results suggest that ether and restraint stress elevate plasma CRH shortly after the onset of the stress, and that this elevation in the plasma CRH level is at least partly responsible for stress-induced ACTH secretion.
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PMID:Effect of acute ether or restraint stress on plasma corticotropin-releasing hormone, vasopressin and oxytocin levels in the rat. 254 72

1. Coexisting with oxytocin or vasopressin in the cell bodies and nerve terminals of the hypothalamic-neurohypophysial system are smaller amounts of other peptides. For a number of these "copeptides" there is strong evidence of corelease with the major magnocellular hormones. Guided by the location of their specific receptors we have studied the effects of three copeptides, dynorphin, cholecystokinin (CCK), and corticotropin releasing hormone (CRH), on the secretion of oxytocin and vasopressin from isolated rat neural lobe or neurointermediate lobe preparations in vitro. 2. Dynorphin is coreleased with vasopressin from neural lobe nerve terminals and acts on neural lobe kappa-opiate receptors to inhibit the electrically stimulated secretion of oxytocin. Naloxone augments oxytocin release from the neural lobe in a manner directly proportional to the amount of vasopressin (and presumably dynorphin) released. 3. Cholecystokinin, coreleased with oxytocin by neural lobe terminals, has been shown to have high-affinity receptors located in the NL and to stimulate secretion of both oxytocin and vasopressin. CCK's secretagogue effect was independent of electrical stimulation and extracellular Ca2+ and was blocked by an inhibitor of protein kinase C. 4. CRH, coreleased with OT from the neural lobe, has receptors in the intermediate lobe of the pituitary, but not in the neural lobe itself. CRH stimulates the secretion of oxytocin and vasopressin from combined neurointermediate lobes but not from isolated neural lobes. Intermediate lobe peptides, alpha and gamma melanocyte stimulating hormone, induced secretion of oxytocin and vasopressin from isolated neural lobes. Their effect was, like that of CCK, independent of electrical stimulation and extracellular Ca2+ and blocked by an inhibitor of protein kinase C. 5. Among the CRH-producing parvocellular neurons of the paraventricular nucleus, in the normal rat, approximately half also produce and store vasopressin. After removal of glucocorticoid influence by adrenalectomy, virtually all of the CRH neurons contain vasopressin. 6. The two subtypes of CRH neurosecretory cells found in the normal rat possess different topographical distributions in the paraventricular nucleus, suggesting the possibility of differential innervation. Stress selectively activates the vasopressin containing subpopulation of CRH neurons, indicating that there are separate channels of regulatory input controlling the two components of the parvocellular CRH neurosecretory system.
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PMID:Coexisting peptides in hypothalamic neuroendocrine systems: some functional implications. 257 30

The data highlighted here suggest that the CRH effects of vasopressin and oxytocin are mediated by one and the same hypophysial receptor which has unique pharmacological specificity. The nomenclature for this receptor type is not established; both V3(53) and V1 beta 39 have been proposed. The former proposal is logical if the pharmacology of ligand recognition is emphasized, whereas the latter designation takes into account that transmembrane signalling from V1 receptors occurs via coupling proteins Go and Gi but not Gs. Such issues are best resolved after cDNA cloning of the genes for the receptors: in the meanwhile the working definition V3 seems more convenient. Several studies show that pituitary V3 receptors are regulated by the concentration of vasopressin in hypophysial portal blood and the amount of glucocorticoid hormones in the circulation (see Ref. 9 for review). Work in this area should clarify further the intracellular mechanism of the CRH action of vasopressin, as well as the factors that determine the responsiveness of corticotrophs to various secretagogues. Most recently, it has been shown that vasopressin is a potent thyrotropin-releasing hormone. This finding extends further the growing concept that there is considerable "cross-talk" between the classical neuroendocrine axes. These were previously thought to be separated by the hypothalamic organization of "final common pathways" of neuroendocrine motoneurons in the hypothalamus, each producing a unique neurohormone to regulate a single type of adenohypophysial cell. It seems that the days of the validity of this hypothesis are numbered, and an important task will be to determine the possible physiological significance of the "cross-talk" within the hypothalamo-pituitary unit in the regulation adrenocortical function.
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PMID:Receptors mediating the CRH effects of vasopressin and oxytocin. 283 75

Human placenta contains the POMC-derived peptides ACTH, alpha MSH, and beta-endorphin, and CRH. High concentrations of immunoreactive (IR) CRH have been recently demonstrated in maternal plasma during pregnancy. To determine if the human placenta secretes CRH and POMC-derived peptides, we developed an in vitro human placental fragment perifusion system. The perifused tissue released IR-CRH and POMC-derived peptides at a constant rate for at least 5 h. The mean IR-CRH concentration in the effluent (under basal conditions) was 158 +/- 26 (+/- SD) pg (34.5 +/- 5.8 fmol)/5-min fraction.g tissue. IR-alpha MSH, IR-beta-endorphin, and IR-ACTH were also released into the perifusion medium; the mean concentration of alpha MSH released was 24.6 +/- 8 pg (14.8 +/- 4.8 fmol)/fraction.g, that of ACTH was 2.9 +/- 1.9 pg (0.65 +/- 0.43 fmol)/fraction.g, and that of beta-endorphin was 12.9 +/- 6 pg (3.8 +/- 1.7 fmol)/fraction.g. We examined the effects of human CRH, oxytocin, vasopressin, and dexamethasone on placental POMC peptide secretion. Five-minute pulses of 10(-8) or 10(-6) mol/L human CRH or oxytocin produced an immediate and dose-dependent increase in all POMC peptides in the effluent. A 5-min pulse of 10(-8) or 10(-6) mol/L vasopressin had no effect. A continuous 4-h exposure to 10(-6) mol/L dexamethasone had no effect on either basal IR-CRH or POMC-derived peptide or their KCl-induced release. In conclusion, we found that 1) human placenta releases IR-CRH and POMC-derived peptides in vitro; this phenomenon seems to be independent of glucocorticoid control; 2) placental CRH may have a paracrine effect on placental POMC peptide release in addition to its possible action on maternal pituitary hormone release; and 3) oxytocin, but not vasopressin, stimulates placental POMC peptide release.
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PMID:Corticotropin-releasing hormone and oxytocin stimulate the release of placental proopiomelanocortin peptides. 283 12

Luteinizing hormone releasing hormone (LHRH) neurons from the preoptic area (POA)/hypothalamus of the postnatal rat were cultured for up to 7 weeks using a slice explant roller culture technique. The slices thinned to quasi-monolayers, but maintained organotypic distributions of large numbers of immunocytochemically identifiable LHRH, neurotensin, tyrosine hydroxylase, neurophysin and corticotropin releasing hormone-containing neurons. The distribution, survival and morphology of LHRH cells in co-cultures with brainstem and anterior pituitary was quantitated, and found to be similar to that observed in single cultures. LHRH fibers grew into either pituitary or brainstem tissue, however when all three tissues were co-cultured, LHRH fibers preferentially invaded the pituitary. LH immunoreactive anterior pituitary gonadotropes were maintained only in co-cultures containing POA/hypothalamic slices, and addition of an LHRH antagonist in such cultures, inhibited LH immunoreactivity in the gonadotropes. This slice explant roller culture method effectively maintains the cyto- and chemoarchitecture and functional properties of the LHRH system for long periods in vitro and should provide excellent models for studying the interactive and molecular characteristics of postnatal LHRH neurons.
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PMID:Slice cultures of LHRH neurons in the presence and absence of brainstem and pituitary. 307 35

A sex steroid hormone sensitive brainstem-allocortex axis of neuronal cell groups and projections is recognized with convergent pathways of aminergic-peptidergic messenger systems, which subserves the adjustment for varying reproductive and environmental conditions and the coordination of endocrine-autonomic functions. Main stations in the A-B-C (Allocortex-Brainstem-Core) periventricular axis include the substantia gelatinosa, nucleus (n.) tractus solitarii-dorsal vagal nucleus-area postrema complex, locus ceruleus, n. parabrachialis, central gray and associated raphe nuclei, ventral tegmental area, lateral and periventricular hypothalamus, n. paraventricularis, bed nucleus of the stria terminalis, preoptic-septal nuclei and n. centralis amygdalae with associated amygdaloid nuclei, as well as the ventral and dorsal allocortex. All of these stations and their periventricular and medial forebrain bundle projections contain estradiol sites of action and represent elements of earlier defined periventricular estradiol-target neuron systems. Results from colocalization of 3H estradiol by thaw-mount autoradiography and aminergic and peptidergic messengers by immunohistochemistry or other histochemical techniques indicate direct nuclear effects of estradiol on certain noradrenalin, dopamine, gamma aminobutyric acid, somatostatin, and neurophysin neurons. Additional data about correspondence of estradiol-target neuron accumulations with neuronal sites of peptide messenger production suggest direct effects of estradiol on certain enkephalin, endorphin, corticotropin releasing hormone, adrenalin, serotonin, cholecystokinin, pancreatic polypeptide and gonadotropin releasing hormone neurons--and probably others. As documented for the pituitary, and as an approach to understand varying and dual effects, it is postulated that estradiol activation of brain messenger systems parallels the heterogeneous estradiol binding in the A-B-C- system. This is expressed in the concept of differential Multiple Activation of Heterogeneous Systems (MAHS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The A-B-C (Allocortex-Brainstem-Core) circuitry of endocrine-autonomic integration and regulation: a proposed hypothesis on the anatomical-functional relationships between estradiol sites of action and peptidergic-aminergic neuronal systems. 638 51

Using probes for rat neural nitric oxide synthase (NOS) mRNA and GnRH mRNA, we performed in situ hybridization to survey NOS mRNA distribution within the hypothalamus of the male and female rat and sought evidence for its expression in GnRH neurons. The NOS cRNA probe was radiolabelled with 35S, and a digoxigenin-labeled rat GnRH cRNA probe was used for double-label studies. NOS mRNA was localized in discrete hypothalamic areas, in grain clusters suggestive of individual neurons. NOS mRNA-positive cells were located mainly in the supraoptic and paraventricular nucleus, particularly overlying the magnocellular division. Rostrally, cells expressing NOS mRNA were especially prominent in the diagonal band of Broca, in a distribution very similar to GnRH neurons. Nevertheless, only one of 370 cells labeled for GnRH mRNA appeared to be positive for NOS mRNA. We conclude that NOS mRNA is located prominently in regions where CRH, AVP and oxytocin cells are located. NOS mRNA-positive cells are located in close proximity to GnRH neurons, but rarely do such neurons express NOS mRNA.
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PMID:The distribution of hypothalamic nitric oxide synthase mRNA in relation to gonadotrophin-releasing hormone neurons. 751 39

Polysialic acid (PSA) is abundant on growing axons during brain development and down regulated on maturation. However, high amounts of this carbohydrate polymer have been found to persist in some regions of the adult rat brain including the mediobasal hypothalamus. In this study, confocal laser scanning microscopy combined with double fluorescence immunostaining was used to characterize the cellular localization of PSA throughout the median eminence and neurointermediate hypophysial lobe of adult rats. In these regions, polysialic acid-immunoreactivity (PSA-IR) generally appeared associated with fiber-like structures. Double immunostaining experiments demonstrated that, in addition to large axons of the neural lobe immunoreactive to vasopressin or oxytocin, PSA was constantly associated with fibers projecting into the intermediate hypophysial lobe immunoreactive to either gamma-aminobutyric acid (GABA) or tyrosine hydroxylase. Similarly, PSA-IR was detected on most, but not all the fibers immunoreactive to GABA or tyrosine hydroxylase dispersed throughout the neural lobe and the different layers of the median eminence. On the other hand, no PSA-IR was detected on axons immunoreactive to somatostatin or to corticotropin releasing hormone projecting throughout the median eminence, or on glial cell bodies and processes immunoreactive for glial fibrillary acidic protein (GFAP) or for vimentin dispersed throughout the median eminence and the neural lobe.
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PMID:Immunolocalization of polysialic acid in the median eminence and neurointermediate hypophysial lobe of adult rats. 789 19

This paper reviews the recent progress in the understanding of the neurobiology of the eating disorders. The analysis of the biochemical abnormalities present in the patients with bulimia nervosa indicates the decrease of central serotonin and noradrenalin activity, elevation of the levels of cerebrospinal fluid peptide YY, alterations of the endogenous opioids and also reduction of peripheral cholecystokinin levels. As these studies were performed on patients who were actively binging and purging it is conceivable that the above abnormalities can results from a pathological feeding pattern. It is also suggested that the reduction of central serotoninergic activity is the stable, trait-related dysregulation of neurotransmitter system activity. In patients with anorexia nervosa the endocrine disturbances of the hypothalamic-pituitary-ovarian and hypothalamic-pituitary-adrenal axes were thoroughly studied. Underweight anorectic patients have been found to have elevations of cerebrospinal fluid level of neuropeptide Y, corticotropin releasing hormone and vasopressin as well as reductions of beta-endorphin and oxytocin level. However, most of the neuropeptide alterations normalize following weight recovery. The only exception is a persistent increase of central serotonin activity postulated to be responsible for the obsessive-compulsive personality traits and disturbed eating behaviors found in these patients.
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PMID:[Selected issues of biological aspects of eating disorders]. 799 11


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