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 excitatory neurotransmitter, L-glutamate (0.5 M, pH 7.4), or the organic acid, acetate (0.5 M, pH 7.4), was microinjected (50 nl over 2 min) directly into the paraventricular nuclei (PVN) of pentobarbital sodium-anesthetized rats while arterial blood pressure and heart rate and plasma adrenocorticotropic hormone (ACTH), vasopressin, and oxytocin were measured. Activation of PVN neurons with L-glutamate led to increases in plasma ACTH, vasopressin, and oxytocin and a profound bradycardia (approximately 80 beats/min) with little change in arterial blood pressure. Microinjection of acetate had no effect on the above variables. The decrease in heart rate was shown to be dependent on the concentration of glutamate injected and the volume of injectate. The bradycardia was mediated through the autonomic nervous system because ganglionic blockade (pentolinium tartrate) eliminated the response; atropine and propranolol severely attenuated the bradycardia. The bradycardia was greatest when L-glutamate was microinjected into the caudal PVN. Injections into the rostral PVN or into nuclei surrounding the PVN led to small or nonsignificant decreases in heart rate. Focal electric stimulation (2-50 microA) of the PVN also led to decreases in heart rate and arterial blood pressure. These data suggest that activation of PVN neurons leads to the release of ACTH, vasopressin, and oxytocin from the pituitary and a bradycardia that is mediated by the autonomic nervous system.
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PMID:Paraventricular stimulation with glutamate elicits bradycardia and pituitary responses. 256 5

The neurohumoral changes induced by electroconvulsive therapy (ECT) in pregnancy have not been described previously. In the nonpregnant adult, ECT causes an acute rise in prolactin, adrenocorticotropic hormone (ACTH), cortisol, norepinephrine, epinephrine and beta-endorphin. Because pregnancy alters the production and release of these hormones, consideration should be given to how ECT may further alter the neuroendocrine response, with possible implications for the success of treatment and the fetal response. A 30-year-old woman with a major affective disorder underwent a course of ECT beginning at 23 weeks' gestation. Serial hormonal assays of peripheral venous samples from -30 to +240 minutes were obtained during her first treatment. The prolactin, ACTH, norepinephrine, epinephrine, beta-endorphin, dopamine and oxytocin levels rose acutely and returned to baseline during observation. The maternal vital signs were stable. No increase in uterine activity or fetal heart rate abnormalities were observed during any treatment. A healthy infant weighing 2,900 g was delivered at term, with Apgar scores of 9 and 9 and no problems. We conclude that there are acute neurohumoral changes in specific hormones with ECT in pregnancy, but none of these changes appeared to adversely affect the fetus in our case.
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PMID:Acute neurohumoral response to electroconvulsive therapy during pregnancy. A case report. 257 26

Vasopressin (AVP) and oxytocin (OT) are hypothalamic neuropeptides having distinct peripherally and centrally directed cell populations. While principally responsible for the regulation of osmotic equilibrium, AVP also participates in stress-mediated adrenocorticotropic hormone (ACTH) release, and in consolidation and retrieval of aversively conditioned behaviors. OT is principally known for its role in parturition and lactation, but also has effects opposite of AVP, antagonizing stress-mediated ACTH release and impairing the consolidation and retrieval of aversively conditioned behaviors. Our group has demonstrated novel peripheral osmoregulatory defects in underweight anorexics, coupled with hypersecretion of AVP into the cerebrospinal fluid (CSF). Conversely, a relative reduction of CSF OT is seen in underweight anorexics. Speculatively, these reciprocal changes in neurohypophyseal peptides in the underweight anorexic may enhance the observed neuroendocrine and cognitive abnormalities. In addition, the alterations in CSF OT may occur as a consequence of the abnormal gastrointestinal function present during the acute stages of anorexia nervosa.
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PMID:Neurohypophyseal dysfunction: implications for the pathophysiology of eating disorders. 269 13

The effect of electrolytic lesion of the paraventricular nucleus of the hypothalamus (PVN) on yawning and penile erection induced by apomorphine, oxytocin and adrenocorticotropic hormone (ACTH1-24) was studied in male rats. In sham-operated rats, apomorphine (50 micrograms/kg s.c.), oxytocin (30 ng i.c.v.), and ACTH1-24 (10 micrograms i.c.v.) significantly increased the number of yawning and penile erection episodes. In PVN-lesioned rats, apomorphine- and oxytocin-, but not ACTH-induced responses were strongly reduced. These results confirm our previous observations showing that the PVN has a crucial role in the expression of yawning and penile erection induced by dopamino-mimetic drugs and oxytocin, and suggest that ACTH-derived peptides induce the above responses by a mechanism not involving PVN hypothalamic dopamine or oxytocin.
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PMID:Paraventricular nucleus lesion prevents yawning and penile erection induced by apomorphine and oxytocin but not by ACTH in rats. 282 10

The direct effect of vasopressin on adrenal steroidogenesis and its effect on angiotensin II- and adrenocorticotropic hormone (ACTH)-stimulated steroidogenesis was evaluated by using an isolated perfused canine adrenal gland preparation. Infusions of vasopressin alone (50, 100, or 250 pg/ml perfusate) had no significant effect on the secretion of either aldosterone or cortisol. Infusions of vasopressin at 75 or 250 pg/ml perfusate during stimulation of steroidogenesis by angiotensin II or by ACTH did not cause a consistent increase in aldosterone secretion. In contrast, infusion of 250 but not 75 pg vasopressin/ml perfusate caused a consistent enhancement of ACTH-stimulated cortisol secretion. The infusion of a vasopressin V1-receptor agonist, but not of either a vasopressin V2-receptor agonist or oxytocin, also caused a significant enhancement of ACTH-stimulated cortisol secretion. These results suggest that the sensitivity of fasciculata cells to vasopressin is greater than that of glomerulosa cells. Finally, levels of vasopressin reported to occur in plasma during severe hemorrhage appear to be capable of enhancing cortisol secretion by a direct action on the adrenal gland via a V1-receptor mechanism.
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PMID:Effect of vasopressin on adrenal steroidogenesis. 284 63

The anteroventral periventricular nucleus (AVPv), which lies in the periventricular zone of the preoptic region, is critical for normal phasic gonadotropin secretion since lesions of this nucleus abolish the progesterone-induced surge of luteinizing hormone secretion from the anterior pituitary, block ovulation, and induce persistent vaginal estrus in female rats. However, very little is known about the neurotransmitter-specific pathways associated with this nucleus. In the present study we evaluated the distribution of biochemically specific cells and fibers within the AVPv and adjacent regions by using an indirect immunohistochemical method with antisera to serotonin (5-HT), dopamine beta-hydroxylase (DBH), tyrosine hydroxylase (TH), neuropeptide Y (NPY), cholecystokinin-8 (CCK), vasoactive intestinal polypeptide (VIP), substance P (SP), neurotensin (NT), corticotropin-releasing factor (CRF), luteotropin-releasing hormone (LRH), somatostatin (SS), thyrotropin-releasing hormone (TRH), oxytocin (OXY), vasopressin (VAS), adrenocorticotropic hormone (ACTH1-24), alpha-melanocyte-stimulating hormone (alpha-MSH), leucine-enkephalin (L-ENK), and calcitonin gene-related peptide (CGRP). Our findings indicate that both cells and fibers containing these putative neurotransmitters are differentially distributed in and around the AVPv in accordance with the cytoarchitectonic organization of this part of the preoptic region. The AVPv itself appears to receive strong inputs from SP-, VAS-, CCK-, and SS-containing pathways, whereas the highest densities of L-ENK-, NT-, 5-HT-, NPY-, and DBH-immunoreactive fibers were found in the cell-sparse zone just lateral to the AVPv. The suprachiasmatic preoptic nucleus (PSCh), a small group of cells located ventral to the AVPv just dorsal to the optic chiasm, contained high densities of alpha-MSH- and ACTH-immunoreactive fibers, as well as substantial numbers of fibers containing catecholamines or NPY. In contrast, a dense plexus of VAS-stained fibers was distributed fairly evenly throughout the AVPv and PSCh. Numerous L-ENK-immunoreactive cell bodies, and moderate numbers of CCK-, NT-, and CRF-stained cell bodies were found in the AVPv. The PSCh contained many TH-stained cells (presumably dopaminergic), in addition to a moderate number of CCK-containing cell bodies, while a high density of NT- and CRF-stained cells were found in the cell-sparse zone lateral to the AVPv, in addition to several CCK-, SP-, VIP-, and TH-containing cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The distribution of neurotransmitter-specific cells and fibers in the anteroventral periventricular nucleus: implications for the control of gonadotropin secretion in the rat. 288 Jun 34

To investigate catecholamine regulation of adrenocorticotropic hormone (ACTH) and vasopressin (VP) release, the relationship of alpha-adrenergic receptor-binding sites to corticotropin-releasing factor (CRF) and VP-containing cell populations within the paraventricular nucleus (PVN) of the hypothalamus was studied. Immunohistochemistry for CRF and neurophysin-vasopressin (NP-VP) was combined with receptor autoradiography. The adrenergic antagonist [3H]-prazosin was used to visualize alpha-1-binding sites and the agonist [3H]-p-aminoclonidine to visualize alpha-2-binding sites. To determine if changes in adrenergic binding accompanied experimentally induced increased activity of CRF- and VP-containing neurons, adrenalectomy was used as a stimulus for CRF release and dehydration as a stimulus for VP release. Quantitative assessment of autoradiograms revealed a greater density of alpha-1- and alpha-2-binding sites over the medial, parvocellular, CRF-containing region of PVN as compared to the lateral, magnocellular, NP-VP-containing region of the nucleus in all animal groups. Following 10 days of dehydration, the density of alpha-1- and alpha-2-binding sites associated with the CRF- and NP-VP-containing regions of PVN decreased. At 14 days postadrenalectomy the density of alpha-2-binding sites associated with CRF- and NP-VP-containing regions of the nucleus decreased, but the density of alpha-1-binding sites was unchanged. Results of this study support the hypothesis that epinephrine and/or norepinephrine regulate the release of ACTH and vasopressin via alpha-1- and alpha-2-adrenergic receptors associated with CRF- and VP-containing somata within the PVN.
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PMID:Relationship of alpha-1- and alpha-2-adrenergic-binding sites to regions of the paraventricular nucleus of the hypothalamus containing corticotropin-releasing factor and vasopressin neurons. 289 48

We studied five cases of central nervous system neuronal tumor, one gangliocytoma and four gangliogliomas, both ultrastructurally and immunohistochemically, using antibodies to neuroendocrine markers including tyrosine hydroxylase (TH), serotonin (5HT), somatostatin (SOM), met-enkephalin (MEK), leu-enkephalin (LEK), substance P (SP), gastrin, vasopressin, oxytocin, vasoactive intestinal polypeptide, adrenocorticotropic hormone and calcitonin. In all cases, the presence of dense-core vesicles (60-250 nm) in the neuronal elements was the characteristic ultrastructural finding. Synapses were observed in two cases. Immunohistochemically, variable numbers of neuronal cells showed positive staining for SOM in five cases, TH, MEK and LEK in three cases, and 5HT and SP in one case each. The others were negative. Positive immunoreactivity for multiple markers was shown in all cases. SOM, TH, 5HT and SP were present in the small- to medium-sized cells, while MEK and LEK were almost exclusively confined to the large cells. Our study clearly indicated that these tumors contained neuronal cells which were not homogeneous with regard to neuroendocrine markers.
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PMID:Neuroendocrine markers in central nervous system neuronal tumors (gangliocytoma and ganglioglioma). 292 88

Neurophysins have been recognized as the carrier proteins of vasopressin and oxytocin. The distribution of neurophysins is immunohistochemically confirmed in the hypothalamus, median eminence, and posterior lobe of the pituitary gland. The authors detected neurophysins in the human corticotrophs and pituitary adenomas with the use of the immunohistochemical method with antiserum to human neurophysins, which did not cross-react with adrenocorticotropic hormone (ACTH), beta-endorphin, and corticotropin-releasing factor. All of ten pituitary glands obtained by autopsy revealed the presence of neurophysin-positive cells in the anterior, intermediate, and the posterior lobes. The neurophysin-positive cells were similar to the corticotrophs in shape and distribution. Simultaneous staining for ACTH and neurophysins in the serial sections revealed that neurophysin-positive cells were also ACTH-positive. One hundred twenty-four cases of pituitary adenoma operated upon were investigated. All of 7 Cushing's adenomas were composed of neurophysin-positive cells. Six tumors with giantism showed sparsely distributed neurophysin-positive cells. No neurophysin-positive cells were observed in any other cases. This study is the first reported evidence of the presence of neurophysins in the human corticotrophs and pituitary adenomas.
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PMID:Presence of neurophysins in the human pituitary corticotrophs, Cushing's adenomas, and growth hormone-producing adenomas detected by immunohistochemical study. 302 92

The hypothalamic-pituitary-adrenocortical axis is activated in pregnancy and parturition. Levels of immunoreactive corticotrophin releasing factor (irCRF), immunoreactive adrenocorticotropic hormone (irACTH) and cortisol concentrations in maternal plasma are elevated throughout gestation, increase further during labour and fall precipitously after parturition. The placenta contains biologically active CRF and ACTH and it has been suggested that the placenta produces these peptides during pregnancy. Here we show that irCRF is located in the cytotrophoblast cells of placenta collected at term. Using a monolayer primary culture of human placental cells we have found that CRF stimulates secretion of peptides containing the ACTH sequence in the placenta in a dose-dependent manner, as it does in the pituitary. This effect is reversed by a CRF antagonist and is mimicked by dibutyryl cyclic AMP and forskolin. Glucocorticoids, which suppress the secretion of pituitary ACTH, were found to have no influence on release of irACTH by the placenta. Oxytocin and prostaglandins stimulate irACTH and irCRF secretion from cultured placental cells and the irACTH-releasing activity of two prostaglandins is partially reversed by a CRF antagonist. Thus CRF may be involved in the paracrine regulation of placental irACTH secretion.
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PMID:Evidence for local stimulation of ACTH secretion by corticotropin-releasing factor in human placenta. 303 77


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