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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arginine vasopressin (AVP), oxytocin (OT), and angiotensin-II (AII) elicit a biphasic ACTH secretory response by perifused anterior pituitary cells consisting of an initial transient (less than 3-min) spike phase and a subsequent sustained plateau phase. In contrast, CRF produces a monophasic sustained plateau type of ACTH secretory response. We have previously demonstrated that 1) influx of extracellular Ca2+ (Cae2+) via L-type voltage-sensitive Ca2+ channels is involved in both the response to CRF and the sustained phase of the response to AVP and OT; 2) release of intracellular Ca2+ (Cai2+) is involved in the spike phase of the response to AVP, OT, and AII; and 3) activation of protein kinase-C is required for the sustained phase, but not for the spike phase, of the response to AVP. CRF action is mediated by activation of protein kinase-A. In this study we further examined the role of Cai2+ by exploiting the fact that a low concentration (1 microM) of ionomycin, a potent Ca2+ ionophore, releases Cai2+ from nonmitochondrial inositol-1,4,5-trisphosphate (IP3)-sensitive Cai2+ stores without causing Cae2+ influx. Pretreatment with ionomycin for 10 min decreased the spike phase of the response to 100 nM AVP, OT, and AII, but had no effect on the response to 10 nM CRF or the sustained phase of the responses to the other agonists. The combination of CRF plus AVP induced a biphasic and synergistic release of ACTH. Ionomycin pretreatment reduced the spike phase, especially the first 1 min, without any effect on the sustained phase. These results indicate that Cai2+ release, but not Cae2+ influx, is involved in the spike phase of the response to AVP, OT, and AII and that Cai2+ is not involved in the synergistic effect of the combination of CRF plus AVP. Having established these relationships, we examined the effect of 2-h perifusion with 100 nM dexamethasone (DEX) on stimulated ACTH release. DEX pretreatment reduced the total response to CRF, the sustained phase of the responses to AVP and OT, and the sustained phase of the synergistic response to CRF plus AVP. However, DEX had no effect on the spike phase of the responses to AVP, OT, or AII or the spike phase of the response to CRF plus AVP. These results indicate that DEX inhibits ACTH release mediated by activation of either protein kinase-A or protein kinase-C, but does not affect inositol-1,4,5-trisphosphate/Cai2(+)-mediated ACTH release.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of intracellular Ca2+ depletion and glucocorticoid on stimulated adrenocorticotropin release by rat anterior pituitary cells in a microperifusion system. 184 62

To examine the relationship between corticotrophin releasing hormone (CRH), arginine vasopressin (AVP) and oxytocin (OXT) we have studied the responses of adenohypophyseal and neurohypophyseal hormones to CRH in eight patients (age 26-64 years, six female) with suspected pituitary-dependent Cushing's syndrome during bilateral, simultaneous inferior petrosal sinus catheterization. Blood samples were taken from both petrosal sinuses and a peripheral vein before, and at 5-min intervals for 15 min after, an intravenous injection of 100 micrograms human CRH1-41. CRH increased sinus AVP concentrations in all eight patients and OXT concentrations in four of five patients studied. Although AVP concentrations often increased in both sinuses, the side of maximal AVP rise was termed side(max-AVP). CRH did not affect peripheral or petrosal sinus mean concentrations of LH, FSH, GH or TSH. While there was no change in mean peripheral concentrations of AVP, OXT, ACTH, ACTH precursors or prolactin after CRH, sinus concentrations of OXT, ACTH and prolactin on side(max-AVP) were markedly elevated over contralateral values. CRH did not increase mean sinus concentrations of ACTH precursors. In seven patients with either no radiological abnormality or the pituitary fossa or a small adenoma the mean ACTH precursor/ACTH ratio in blood sampled from all sites was 2.1 +/- 0.16 (mean +/- SEM, n = 50). In a patient with a large, locally invasive tumour the mean ACTH precursor/ACTH molar ratio was 32.1 +/- 1.3 (n = 12; P less than 0.001), suggesting that alterations in this molar ratio may reflect the biological properties of the tumour. The source of CRH-stimulatable AVP and OXT remains uncertain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Corticotrophin releasing hormone (CRH1-41) stimulates the secretion of adrenocorticotrophin, vasopressin and oxytocin but not adrenocorticotrophin precursors: evidence from petrosal sinus sampling in man. 184 86

Bilateral adrenalectomy (ADX) leads to increased ACTH synthesis and secretion. It is thought that endogenous glucocorticoids exert a feedback mechanism at both pituitary and brain levels. The present study has been performed in order to determine the effect of ADX on the release of hypothalamic neuropeptides with corticotropin-releasing activity (CRA) and if there exists a median eminence site of glucocorticoid action to regulate hypothalamic-pituitary-adrenal (HPA) function. Adrenalectomized and sham-operated male rats were killed at different periods after surgery (2, 5, 7 and 14 days) and trunk blood was collected for ACTH and corticosterone (B) concentrations measurement. Brain (median eminence, ME; and medial basal hypothalamus, MBH) and pituitary (anterior lobe, AP; and neurointermediate lobe, NIL) tissues were dissected in order to evaluate either peptide content or in vitro hormone release. The results indicate that ADX blunted plasma B levels and increased AP ACTH content and secretion in a time-related fashion up to the 14th day. ADX significantly decreased both CRF and CRA contents in the ME at all periods studied; ME arginine-vasopressin (AVP) increased 7 and 14 days after ADX. MBH CRF decreased after ADX, but returned to sham value 2 weeks later; similarly, MBH AVP decreased at all periods after ADX. Removal of endogenous glucocorticoids did not vary neither oxytocin (OXY) content in the ME and MBH nor AVP and OXY contents in the NIL. In our superfusion experiments, we found that ADX increased basal AVP release and did not change spontaneous CRF secretion from ME terminals. Dexamethasone (Dxm, 10 nM) diminished AVP but not CRF output by ME tissues from adrenalectomized rats. A direct relationship was found between ME CRF and 28 mM KCl (hK+)-induced CRF release by MEs from adrenalectomized rats. ME fragments from adrenalectomized rats were hyperresponsive to kH+ stimulation of AVP release. Dxm (10 nM) decreased the hK(+)-evoked CRF and AVP release by MEs from adrenalectomized rats. ADX and dexamethasone treatment did not influence basal and hK(+)-elicited ME OXY release. Additionally, a rapid glucocorticoid inhibitory effect on ACTH secretion by isolated AP cells from both sham and adrenalectomized rats was found, and an in vitro corticotrope hyporesponse to 0.63 nM CRF and 9.25 nM AVP stimulation during several days after ADX.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in the hypothalamo-corticotrope axis after bilateral adrenalectomy: evidence for a median eminence site of glucocorticoid action. 184 20

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

Oxytocin has been suggested to have glucoregulatory functions in rats, man and other mammals. The hyperglycemic actions of oxytocin are believed to be mediated indirectly through changes in pancreatic function. The present study examined the interaction between glucose and oxytocin in normal and streptozotocin (STZ)-induced diabetic rats, under basal conditions and after injections of oxytocin. Plasma glucose and endogenous oxytocin levels were significantly correlated in cannulated lactating rats (r = 0.44, P less than 0.01). To test the hypothesis that oxytocin was acting to elevate plasma glucose, adult male rats were injected with 10 micrograms/kg oxytocin and killed 60 min later. Oxytocin increased plasma glucose from 6.1 +/- 0.1 to 6.8 +/- 0.2 mM (P less than 0.05), and glucagon from 179 +/- 12 to 259 +/- 32 pg/ml (P less than 0.01, n = 18). There was no significant effect of oxytocin on plasma insulin, although the levels were increased by 30%. A lower dose (1 microgram/kg) of oxytocin had no significant effect on plasma glucose or glucagon. To eliminate putative local inhibitory effects of insulin on glucagon secretion, male rats were made diabetic by i.p. injection of 100 mg/kg STZ, which increased glucose to greater than 18 mM and glucagon to 249 +/- 25 pg/ml (P less than 0.05). In these rats, 10 micrograms/kg oxytocin failed to further increase plasma glucose, but caused a much greater increase in glucagon (to 828 +/- 248 pg/ml) and also increased plasma ACTH. A specific oxytocin analog, Thr4,Gly7-oxytocin, mimicked the effect of oxytocin on glucagon secretion in diabetic rats. The lower dose of oxytocin also increased glucagon levels (to 1300 +/- 250 pg/ml), but the effect was not significant. A 3 h i.v. infusion of 1 nmol/kg per h oxytocin in conscious male rats significantly increased glucagon levels by 30 min in normal and STZ-rats; levels returned to baseline by 30 min after stopping the infusion. Plasma glucose increased in the normal, but not STZ-rats. The relative magnitude of the increase in glucagon was identical for normal and diabetic rats, but the absolute levels of glucagon during the infusion were twice as high in the diabetics. To test whether hypoglycemia could elevate plasma levels of oxytocin, male rats were injected i.p. with insulin and killed from 15-180 min later. Plasma glucose levels dropped to less than 2.5 mM by 15 min. Oxytocin levels increased by 150-200% at 30 min; however, the effect was not statistically significant.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interactions between oxytocin, glucagon and glucose in normal and streptozotocin-induced diabetic rats. 192 91

This paper summarizes the recent knowledge on the factors stimulating or inhibiting the adrenocortical growth. In the part I of the present review the following stimulatory growth factors are discussed: ACTH--in vivo, N-POMC derivatives, dibutyryl cAMP--in vivo, GH, Prl, vasopressin, oxytocin, insulin, insulin-like growth factor I (somatomedin C), estradiol and vasoactive intestinal polypeptide (VIP). Among the factors, which inhibit the adrenocortical growth, the following ones are considered: ACTH--in vitro, cAMP--in vitro, adrenal steroids and testicular androgens. The remaining hormones and factors affecting the adrenocortical growth are described in the part II of the review.
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PMID:[Factors stimulating and/or inhibiting growth processes of the adrenal cortex. I. The role of the anterior pituitary and hypothalamic hormones, insulin, sex steroids and certain neuropeptides]. 194 99

A survey is given on the regulation of the formation of corticoliberin and of pro-opiomelanocortin and of ACTH, respectively, and on the significance of these compounds. The formation of pro-opiomelanocortin is furthered by corticoliberin, vasopressin, oxytocin and angiotensin II. Receptors for the binding of corticoliberin appear in numerous parts of the central nervous system. In various diseases the content of corticoliberin in the plasma and in certain tissues is changed. The inhibition of the ACTH secretion by glucocorticosteroids takes place via a decrease of the formation of corticoliberin and by a reduction of the equipment of the corticotrophic cells with receptors for its binding. The secretion of corticoliberin and of ACTH, respectively, is increased by loads, by hypoglycaemia, by blood losses, by hypoxia and by infections. In the glucocorticosteroid receptors there are 2 types with different affinity to cortisol and corticosterone.
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PMID:[Current findings in the regulation of formation of corticoliberin, pro-opiomelanocortin and ACTH as well as the efficacy of these compounds]. 196 5

The influence of arginine vasotocin (AVT) on the interrenal secretion of the clawed toad (Xenopus laevis) was studied combining in vivo and in vitro experiments. In vivo: A single injection of 3 nmol AVT per 100 g body weight was given, and the concentrations of corticosterone and aldosterone in the serum were measured after 1, 3, 6, 12, and 24 hr. The serum levels of both steroids remained elevated over 6 hr and declined to normal levels within 12 hr. The increase of the aldosterone concentration was relatively stronger than that of corticosterone. In vitro: A perifusion system was used to study the influence of AVT concentrations ranging from 0.1 to 50 nM on the secretion rates of corticosterone and aldosterone. The response of the interrenals was dose dependent; corresponding to the in vivo results, the elevation rate was higher for aldosterone than for corticosterone. The effects of several nonapeptides were compared. AVT was most effective, followed by mesotocin and arginine vasopressin (AVP). Isotocin and oxytocin had less effect. The selective agonist of the mammalian V2 receptor (1-deamino-8-D-arginine)-vasopressin (DDAVP) did not stimulate the interrenals, while the V1 receptor-selective antagonist ((1-beta-mercapto-beta,beta-cyclopentamethylene propionic acid)-2-(O-methyl)-tyrosine)-AVP could not diminish the stimulation by AVT. Thus, the AVT receptor of the amphibian interrenal must be a special one and is different from the V1 and V2 types of mammals. In a comparison of the effects of AVT with other stimulators such as ACTH(1-28) or urotensin II, it was found that the sensitivity of the interrenals to AVT was similar to that of these peptides. The results indicate that AVT plays an important role in the osmomineral regulation of Xenopus laevis by acting on the corticosteroid secretion of the interrenals.
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PMID:Neurohypophysial hormones and steroidogenesis in the interrenals of Xenopus laevis. 196 9

The role of the paraventricular nuclei (PVN), amygdala and hippocampus in the control of the hypothalamic-pituitary-adrenal axis has been studied by determining the effect of electrical stimulation of the PVN, amygdala and hippocampus on the release of corticotrophin-releasing hormone (CRF-41) and arginine vasopressin (AVP) into hypophysial portal blood and ACTH and corticosterone into peripheral blood. Adult female Wistar rats were anaesthetized with sodium pentobarbitone and stimulation was carried out through previously implanted bipolar, glass-insulated platinum electrodes. Hypophysial portal blood was collected 30 min before and 30 min during the application of the stimulus which consisted of trains (30 s on and 30 s off) of biphasic rectangular pulses with a frequency of 50 Hz, pulse width 1 ms and amplitude 1 mA. Bilateral stimulation of the PVN increased while unilateral stimulation of the amygdala decreased the release of CRF-41 into hypophysial portal blood. The threefold increase in release of CRF-41 induced by PVN stimulation correlated with a marked increase in peripheral plasma concentrations of ACTH and corticosterone. Stimulation of the hippocampus had no significant effect on CRF-41 release, and stimulation of each of the three brain regions had no effect on AVP release into portal blood. These findings were extended in a second study to compare the effects of unilateral bipolar electrical stimulation of the PVN and of the supraoptic nucleus (SON) on the release of CRF-41, AVP and oxytocin. This study was carried out on adult male rats, anaesthetized with sodium pentobarbitone, in which the stimulus was applied through previously implanted concentric stainless-steel electrodes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Corticotrophin-releasing factor-41, vasopressin and oxytocin release into hypophysial portal blood in the rat: effects of electrical stimulation of the hypothalamus, amygdala and hippocampus. 203 Mar 35

The neurotransmitter histamine (HA) participates in the neuroendocrine regulation of pituitary hormone secretion and in the regulation of some peripheral hormones. In general, HA has a stimulatory but indirect effect on the release of these hormones by activation of postsynaptic receptors in the hypothalamic region. The release of the pro-opiomelanocortin-derived peptides ACTH, beta-endorphin (beta-END), and alpha-melanocyte-stimulating hormone (alpha-MSH) occurs by stimulation of H1- and H2-receptors and seems to be mediated via release of corticotropin-releasing hormone and vasopressin from the hypothalamus. The HA-induced release of prolactin (PRL) involves H2-receptors in some hypothalamic areas and H1-receptors in other areas. The release of PRL occurs by histaminergic inhibition of tuberoinfundibular dopaminergic neurons and by stimulation of serotoninergic and vasopressinergic neurons. Histaminergic neurons seem to participate in the mediation of the stress-induced release of ACTH, beta-END, alpha-MSH, and PRL. The neurohypophysial hormones vasopressin and oxytocin are stimulated by HA, and a physiological role of HA in the control of vasopressin secretion is likely. HA stimulates the release of peripheral catecholamines and renin. The stress-induced increase in plasma catecholamines and plasma renin activity (PRA) seems also to involve central histaminergic neurons. The effect of HA and stress on peripheral catecholamines is mediated via H1- and H2-receptors, while that on PRA is mediated via H2-receptors.
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PMID:Neuroendocrine functions of histamine. 205 12


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