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)

Regulation of anterior pituitary secretion of adrenocorticotropin (ACTH) is a complex process subserved by multiple hypophyseotropic factors. The nature of participation (dynamic or permissive) and relative significance of each factor in mediation of stimulus-induced ACTH secretory events have not been elucidated. Attempts were made to directly define the contributions of corticotropin-releasing factor (CRF), arginine vasopressin, oxytocin, and epinephrine to ACTH secretion elicited by hemodynamic and hypoglycemic stimuli in anesthetized rats. The observations support the following hypotheses: 1) CRF represents the predominant regulatory factor in mediation of the stimulus-induced ACTH-secretory responses studied, 2) hypophyseotropic coding of ACTH secretion is stimulus-dependent and involves factors in addition to CRF, and 3) CRF participates in mediation of ACTH secretion in either a dynamic or a permissive fashion depending on the nature of the secretory stimulus. Finally, the potential for central interactions among these regulatory factors is significant and underscores the complexity of this regulatory system at all levels of organization.
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PMID:Hypophyseotropic regulation of adenohypophyseal adrenocorticotropin secretion. 388 Dec 88

Vasopressin (VP) potentiates the effect of corticotropin-releasing factor (CRF) on the secretion of adrenocorticotropic hormone (ACTH) from anterior pituitary cells in vitro, and both CRF and VP have been found in portal blood. These data support the hypothesis that VP acts synergistically with CRF to cause the secretion of ACTH in vivo but the origin of the CRF and VP, and the physiology of their release, have not been precisely defined. Parvocellular cell bodies in the paraventricular nucleus (PVN) which project to the external zone of the median eminence can be stained for both CRF and VP after adrenalectomy, and there is light microscopic immunocytochemical evidence that neurophysin (NP) may be located within some of the CRF-containing axons. Electron microscopic immunocytochemical studies have demonstrated the presence of CRF, VP and its 'carrier' protein, VP-associated neurophysin (NP-VP) in 100-nm neurosecretory vesicles (NSVs) in axons terminating near the portal capillary plexus in the external zone of the median eminence. If these peptides are extensively co-localized in the same NSVs in the median eminence, then coordinate secretion of CRF and VP in vivo is obligatory, at least in some physiological circumstances. We demonstrate in this report, using post-embedding electron microscopic immunocytochemistry on serial ultrathin sections, that CRF, VP and NP-VP are contained not only in the same axons and terminals, but in the same 100-nm NSVs in the median eminence of both normal and adrenalectomized rats. In addition, in the normal rat median eminence 44% of the CRF-positive axons and terminals stained strongly for VP and NP-VP, whereas in the adrenalectomized rat virtually all the CRF-positive structures in the median eminence showed strong staining for VP and NP-VP, indicating a transformation of one subpopulation of CRF-positive axons and terminals by adrenalectomy.
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PMID:Co-localization of corticotropin-releasing factor and vasopressin in median eminence neurosecretory vesicles. 390 Jul 40

Ovine corticotropin releasing factor (oCRF-41) and AVP act synergistically to stimulate pituitary ACTH secretion. In the present study we have investigated whether the effect of AVP, either in the presence or in the absence of oCRF-41 (0.5 nmol/l), could be blocked by V1 (pressor)-antagonists. Furthermore, oxytocin, and [1-deamino,8-D-arginine] vasopressin (dDAVP) were tested for their ability to release ACTH. All experiments were carried out in vitro, using segments of rat anterior pituitary glands. The V1-antagonist [1-deamino,penicillamine(o-methyl-tyrosine)]AVP inhibited ACTH release induced by AVP or AVP + oCRF-41. However, it also had some agonistic activity which was more pronounced in the presence of oCRF-41. An equally potent V1-antagonist, [1-beta-mercapto-beta, beta-cyclopentamethyleneproprionic acid (o-methyl-tyrosine)]AVP, failed to inhibit AVP-stimulated ACTH secretion, and also had weak agonist potency. The relatively selective V2 (antidiuretic)-agonist dDAVP was 20-30 fold less potent than AVP. Oxytocin, a weak V1- and V2-agonist was only 4-8 fold less potent than AVP. These data are compatible with the suggestion that AVP receptors on pituitary corticotrope cells are neither classical V1- nor V2-receptors.
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PMID:Evidence that the effects of arginine-8-vasopressin (AVP) on pituitary corticotropin (ACTH) release are mediated by a novel type of receptor. 608 44

Neonatal treatment with monosodium glutamate (MSG) induces severe neuronal damage in selected brain areas, which in turn results in a number of neuroendocrine abnormalities during adult life. The present study was designed to determine what effects this partial and selective denervation of the hypothalamic-pituitary axis may have on the sensitivity of two key components of that axis, the median eminence (ME) and the anterior pituitary (AP). In order to test any changes in response that may occur after MSG treatment, the release of several peptide hormones from either the ME or the AP was evaluated in vitro, employing specific or general secretagogues. Male newborn pups of the Holtzman strain were injected with MSG every other day for 5 days, starting on day 2 of life; littermate controls received an injection of 10% NaCl. All animals were used when adult, at about 5-7 months of age. After decapitation, ME and AP tissues from control and MSG-treated rats were dissected out and incubated in vitro. Release of LHRH, SRIF, arginine vasopressin, and oxytocin from the ME was measured by direct RIA, under basal conditions and after stimulation with high K+ medium (28 mM). The results clearly indicate a marked hyperresponse of the release of each of the four neuropeptides by ME fragments from MSG-lesioned animals. The altered release was not attributable to changes in ME peptide content. In the case of the AP, the release of ACTH, LH, PRL, and GH in response to high K+ or, in some cases, to specific releasing factors, was evaluated in a dispersed cell preparation. The release of all four protein hormones was increased by high K+, and again the MSG-lesioned rats showed a pronounced hyperresponse. Corticotropin-releasing factor, at concentrations of 10(-9) and 10(-8) M enhanced ACTH release from control and MSG-lesioned rats, but the latter presented a marked hyperresponse. A similar observation on LH release was seen after stimulation with LHRH (10(-9) M). The results indicate that the neuronal damage induced by neonatal MSG treatment results in a generalized hyperresponsiveness in vitro to either specific or general secretagogues by ME or AP tissues, which may suggest the development of a denervation-type supersensitivity in the hypothalamic-pituitary axis. Since the release of these peptide hormones is sluggish in MSG-lesioned rats under in vivo conditions, it seems plausible to conclude that the major defect after the neurotoxin damage may reside in the loss of neurotransmitter systems normally innervating and regulating the activity of the peptidergic neurons.
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PMID:Increased responsiveness of the hypothalamic-pituitary axis after neurotoxin-induced hypothalamic denervation. 614 82

In diabetes insipidus (DI) rats, electrical stimulation of the posterior pituitary lobes in vitro promotes the release of corticotropin-releasing factor (CRF). The CRF activity is abolished by preincubation of the posterior lobe media with thioglycolate. Oxytocin, which is released concomitantly into the medium (3.2 mIU/lobe/20 min), accounts for the complete CRF effect. Neural lobe extracts from DI and normal rats contain 40-70% more CRF activity than can be explained by their content in vasopressin and/or oxytocin. The discrepancy between released and extracted CRFs suggests that hypothetical CRFs or potentiating factors are not released from nerve endings or have to be present in high concentrations to manifest their effect.
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PMID:Oxytocin: major corticotropin-releasing factor secreted from diabetes insipidus rat posterior pituitary in vitro. 625 96

To study the role of the paraventricular nucleus and of neurohypophysial hormones in the control of ACTH secretion, the paraventricular nuclei (PV) of Brattleboro diabetes insipidus rats (DI) were lesioned (L) with a knife; sham-lesioned DI (S) served as controls. Four days later, the rats were stressed by ether inhalation, and blood samples were taken during and 30-40 min after stress for the determination of corticosterone. The median eminence (ME) and neural lobe (NL) were homogenized in 50 microliters of 0.1 N HCl and frozen pending bioassay of corticotropin-releasing factor (CRF). PV lesion almost abolished the corticosterone secretion to ether and reduced the ME CRF content three- to sevenfold. The NL CRF content in S was about twice that of ME, and oxytocin accounted for more than 60% of NL CRF. However, PV lesion had no effect on NL CRF activity. Low amounts of oxytocin (2 mU/ml) had no significant CRF activity but potentiated the ME CRF effect in L. The results suggest that 1) PV is one of the most important sites for CRF synthesis or CRF fiber transit in DI; 2) corticosterone secretion to ether stress is governed mainly by ME CRF; and 3) a large proportion of CRF fibers to NL probably originates outside PV.
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PMID:Paraventricular nucleus region controls pituitary-adrenal function in Brattleboro rats. 629 23

Synthetic ovine corticotropin-releasing factor (CRF) is a 41-residue peptide with high potency and intrinsic activity to stimulate the secretion of ACTH and beta-endorphin-like immunoactivity (beta-End-LI) by cultured adenohypophysial corticotropic cells. The action of CRF in vitro can be potentiated by the weaker secretagogues, vasopressin, oxytocin, epinephrine, norepinephrine, and angiotensin II. CRF-mediated secretion of ACTH and beta-End-LI is noncompetitively inhibited by pretreatment of cells with glucocorticoids. Long term exposure of adenohypophysial cells to CRF results in an increase in total medium plus cell ACTH in the cultures, suggesting that CRF can enhance rates of ACTH synthesis as well as release. CRF also stimulates the secretion of beta-End-LI by corticotropic cells cultured from the neurointermediate lobe. Higher concentrations of CRF are required to stimulate secretion by this cell type than by anterior lobe corticotropic cells. These in vitro results are consistent with CRF playing a major physiological role in the neuroregulation of secretion by anterior lobe corticotropic cells, where the peptide may interact with other modulators.
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PMID:Effects of synthetic ovine corticotropin-releasing factor, glucocorticoids, catecholamines, neurohypophysial peptides, and other substances on cultured corticotropic cells. 630 65

The present paper reports new findings concerning interaction of [3H]-Arginine-vasopressin with putative receptors in rat anterior pituitary gland. It shows the presence of a single type of receptor sites, with a limited binding capacity and a dissociation constant of nearly 1nM. The parent neurohormone oxytocin revealed weak affinity as compared with vasopressin [Ki = 100nM and Ki = 1nM, respectively]. None of the various peptides tested and, especially corticotropin-releasing factor CRF, competed for binding. Receptor characteristics appeared to be unaffected by lack of circulating vasopressin in Brattleboro rats presenting complete deficiency in synthesis of that peptide.
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PMID:Characterization of specific receptors for vasopressin in the pituitary gland. 631 81

We have investigated the effects of synthetic oxytocin and vasopressin on corticotropin release induced by the 41-residue ovine corticotropin-releasing factor (oCRF) in vitro. Segments of the anterior pituitary glands obtained from male and female Wistar or from female hetero- and homozygous Brattleboro rats were used. Ovine CRF (0.1-2.5 nmol/l) stimulated corticotropin release by pituitaries of Wistar rats and this effect was augmented two- to threefold in the presence of arginine vasopressin (0.09-0.9 mIU/ml) or oxytocin (0.9-90 mIU/ml). A similar phenomenon was demonstrated in Brattleboro rats. These data favor the hypothesis that oxytocin might have a physiological role in the regulation of pituitary-adrenocortical function in homozygous Brattleboro rats which lack vasopressin.
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PMID:Oxytocin as well as vasopressin potentiate ovine CRF in vitro. 631 91

To determine if arginine vasopressin (AVP) is involved in the response of ACTH and cortisol (F) to hemorrhage, we examined the effect of injections of AVP-antiserum into the third ventricle in chronically prepared awake cats. Cats were trained to remain unrestrained in a cardboard box. Cats were prepared under halothane and nitrous oxide with aseptic technique. Two to 3 days later, experiments began. Antiserum (5 microliters) to AVP or to oxytocin (OXY) as a control was given 26 min before hemorrhage conducted over 3 min. Thirty minutes after hemorrhage, reinfusion was conducted over 3 min. Each cat received each antiserum in randomized sequence 2-3 days apart. Plasma ACTH and F were measured by RIA. Data were analyzed statistically by analysis of variance. In 12 experiments in 6 cats, ACTH and F increased significantly with 10 ml/kg hemorrhage (P less than 0.01) and to the same extent (P greater than 0.1) after either antiserum. In 20 additional experiments in 10 cats, a submaximal dose of dexamethasone was administered sc 2-3 h before hemorrhage of 15 or 17.5 ml/kg. Under this circumstance, ACTH increased significantly (P less than 0.05) after anti-OXY, but not after anti-AVP (P greater than 0.2) so that during hemorrhage the values of ACTH differed significantly (P less than 0.025). F increased significantly more after anti-OXY than after anti-AVP (P less than 0.025). Changes in arterial pressure, heart rate, and plasma glucose with or without pretreatment with dexamethasone did not differ between groups. Changes in F and ACTH in cats receiving sham injections did not differ from those after anti-OXY. These findings suggest that normally a corticotropin-releasing factor (CRF) or factors act independently of AVP to mediate the response to hemorrhage. However, in the presence of steroid feedback by dexamethasone, the release or action of this CRF(s) is suppressed so that AVP is necessary for a full response. As has been proposed previously by others, AVP could potentiate the action of other CRFs, stimulate their release, or act as a CRF.
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PMID:Effects of vasopressin antiserum on the response of adrenocorticotropin and cortisol to hemorrhage. 631 51


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