UNIPROT:P01178 - FACTA Search

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

Mesenteric artery rings from Wistar and Wistar-Furth rats subcutaneously treated with deoxycorticosterone acetate (DOCA) and 1% NaCl drinking water were used to measure endothelial modulation of contractile sensitivity and vasopressin receptor function and affinity. DOCA-salt hypertension reduced contractile sensitivity to arginine vasopressin (AVP) and did not affect contractile sensitivity to norepinephrine in arteries from Wistar rats. Endothelial removal caused a threefold increase in contractile sensitivity to AVP and norepinephrine in DOCA-salt hypertensive Wistar rats. In Wistar-Furth rats, DOCA-salt treatment did not affect contractile sensitivity to AVP, lysine vasopressin, oxytocin, and norepinephrine or the affinity of the vasopressin receptor for agonists or antagonists. Removal of endothelium did not affect vasopressin contractile sensitivity but caused a 15-fold increase in contractile sensitivity to norepinephrine in untreated or DOCA-salt-treated Wistar-Furth rats. These data show that reduced vasopressin receptor function and increased endothelial function that compensate for increased contractile sensitivity in arteries from DOCA-salt hypertensive Wistar rats are not the cause of resistance of DOCA-salt-treated Wistar-Furth rats to the development of enhanced contractile sensitivity and hypertension.
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PMID:Endothelium, vasopressin receptors, and resistance to DOCA-salt hypertension. 834 27

The acclimation of the clawed toad Xenopus laevis to hyperosmotic solutions of NaCl (balanced solution of sea salt), urea or mannitol was studied. The animals could not be acclimated to salt solutions more concentrated than 400 mosm.1-1. Urea was tolerated till 500 mmol.1-1. Plasma osmolality was always hyperosmotic to the environmental solution, but with diminished osmotic gradient at the highest tolerated solutions. Plasma urea concentration approached 90 mmol.1-1, similar in the three solutions of acclimation. Urine volume was very small under all conditions. Serum aldosterone and corticosterone did not differ significantly, although there was a slight tendency towards lower aldosterone in the NaCl solution. In vivo water uptake in tap water acclimated animals was very small, and was higher in the other groups. Only the salt- and urea-acclimated, but not the tap water and mannitol-acclimated groups responded with a clear increase following injection of oxytocin or theophylline. In vitro urea fluxes were similar and invariable in both directions under all conditions. No significant effect of theophylline was observed. Sodium transport measured by the short-circuit technique in vitro was lower in salt- and mannitol-acclimation conditions, and was stimulated significantly under all conditions in response to serosal oxytocin or theophylline. It is concluded that Xenopus laevis can osmoregulate at a limited range of external solutions. It is limited in the increase of its plasma urea concentration; the transport properties of the skin do not change very much upon acclimation, except for the hydroosmotic response to oxytocin.
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PMID:Mechanisms of hyperosmotic acclimation in Xenopus laevis (salt, urea or mannitol). 834 83

Chronic exposure to a hyperosmolar challenge invokes coordinate, differential, and ostensibly adaptive alterations in the expression of mRNA encoding corticotropin-releasing factor (CRF) in the endocrine hypothalamus. Rats maintained on 2% (wt/vol) saline for 7 days displayed the expected reduction in CRF mRNA levels in the parvocellular neurosecretory compartment of the paraventricular nucleus, as well as a concomitant increase in CRF transcripts in oxytocin-containing magnocellular neurosecretory neurons. Also detected in salt-loaded animals was a prominent induction of the immediate-early gene product Fos in magnocellular neurosecretory cell groups and in several brain regions that are known to provide major projections to the endocrine hypothalamus. These included a triad of cell groups making up the lamina terminalis of the third ventricle, and, to a lesser extent, catecholaminergic cell groups in the caudal brain stem. Discrete transections of descending projections from structures associated with the lamina terminals, as well as excitotoxin lesions centered in one lamina terminalis-associated structure, the organum vasculosum, abolished the effects of salt loading in both the magno- and parvocellular neurosecretory systems. Knife cuts in the lamina terminalis complex that spared only projections from the organum vasculosum region or cuts that disrupted ascending catecholaminergic projections failed to modify either effect of salt loading. The results suggest the existence of a simple circuit through which osmotic influences on gene expression in the magnocellular and parvocellular neurosecretory systems are effected.
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PMID:Mediation of osmoregulatory influences on neuroendocrine corticotropin-releasing factor expression by the ventral lamina terminalis. 835 69

Neuroanatomical and physiological evidence indicates that baroreceptors influence hypothalamic vasopressin (VP) and oxytocin (OT) neurons. We evaluated the effects of sinoaortic denervation (SAD) on the molecular and endocrine response to salt loading. Sham-operated or SAD rats were given a 2% NaCl solution to drink for 72 h. A group with limited salt water intake was included as a second control because the denervated rats consumed less salt than the controls. Plasma VP, OT and osmolality and posterior pituitary peptide content were measured. Brains were processed for evaluation of VP and OT mRNA expression using in situ hybridization with computer quantitation. Salt loading produced equivalent increases in plasma VP and OT in the control and SAD groups, however, there was a greater depletion of posterior pituitary peptides in the denervated animals. Salt loading produced significant decreases in pituitary VP and OT in the SAD animals, 69.8 +/- 8.4% and 68.3 +/- 4.0%, respectively. In the control groups, there was no decrease in VP content and a decrease in OT only in the control ad lib group. The peptide mRNA response to salt loading was also altered in the denervated rats. There was a significant increase in the area and intensity of the labeling for OT mRNA in the PVN in the SAD salt group. The control salt rats showed an increase in the SON and the salt-limited group showed no changes. For VP mRNA, the only change noted was in the SON of the salt-loaded SAD animals. These results show that chronic denervation of arterial baroreceptors augments the hypothalamic VP and OT response to salt loading.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sinoaortic denervation alters the molecular and endocrine responses to salt loading. 836 35

This study demonstrates cholecystokinin receptor plasticity in response to salt-loading in the rat and mouse hypothalamus. It identifies, for the first time, the cholecystokinin receptor subtypes involved, firstly by receptor autoradiography and secondly by in situ hybridization. Both species showed increases in hypothalamic [125I]Bolton Hunter-cholecystokinin-8 binding. Co-incubation with the specific cholecystokininA and cholecystokininB antagonists, devazepide and CI-988, indicated that in the rat cholecystokininB receptor binding markedly increased, with a small increase in cholecystokininA receptor binding. In the mouse the response was comprised solely of cholecystokininA receptors. In situ hybridization studies were carried out on a range of peptide messenger ribonucleic acids after salt-loading. In the rat large increases in hypothalamic gene expression were detected for oxytocin, vasopressin, corticotrophin-releasing factor and preprocholecystokinin. In the mouse only vasopressin messenger ribonucleic acid increased, whilst hypothalamic oxytocin, preprocholecystokinin and corticotropin-releasing factor remained unchanged. However, corticotrophin-releasing factor messenger ribonucleic acid increased in the mouse amygdala. In situ hybridization was performed using oligonucleotide probes specific for either the cholecystokininA or cholecystokininB receptor messenger ribonucleic acid, and this showed good agreement with the receptor autoradiography. CholecystokininB receptor expression was upregulated in the rat hypothalamus along with a small but significant increase in cholecystokininA receptors. In the mouse only cholecystokininA receptor expression was increased. In addition to these molecular changes rats lost about 25% of their body weight during six days of salt-challenge, whilst mice continued to grow in line with controls. This work demonstrates differential changes in cholecystokinin receptor subtype binding between the rat and the mouse. It represents the first report of differential changes in cholecystokininA and cholecystokininB receptor messenger ribonucleic acids within the brain, and shows that cholecystokinin receptors within the rodent hypothalamus are capable of plastic responses to chronic osmotic stress.
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PMID:Changes in hypothalamic cholecystokininA and cholecystokininB receptor subtypes and associated neuropeptide expression in response to salt-stress in the rat and mouse. 857 72

Experiments were performed to evaluate the role of central oxytocin (OT) in the inhibition of salt intake produced by sinoartic denervation (SAD). The effect of OT antisense treatment on 24 h intake of 2% NaCl in SAD and sham-operated (SO) rats was determined. PVN injection of unmodified antisense oligodeoxynucleotides (ODNs) to OT mRNA decreased intake of 2% NaCl in SAD, but not SO rats. Salt consumption was 22 +/- 4 ml after the injection of control ODN as compared to 8 +/- 4 ml after the OT antisense injection (P < 0.05). SAD animals also demonstrated an increased plasma OT response to salt loading, an elevation from 3.2 +/- 0.7 to 6.9 +/- 0.8 pg/ml. In contrast, salt ingestion produced no significant change in plasma OT in the SO group. The increased endocrine response in the SADs occurred even though salt intake was lower in this group. There were no group differences in plasma electrolytes or posterior pituitary OT content. Results show that OT antisense specifically inhibits salt intake in the denervated rat, suggesting that the central oxytocinergic axis stimulates sodium drive in this experimental model.
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PMID:Oxytocin antisense reduces salt intake in the baroreceptor-denervated rat. 858 63

Brain oxytocin (OT) has been suggested to be involved in the inhibition of sodium appetite in the rat. Sodium depleted male rats showed no decrease in sodium intake after they were given a pulse intracerebroventricular (pICV) injection of either OT (1 microgram/microliter) or the selective OT agonist Tyr4-Gly7OT (1 microgram/microliter). Administration of the OT selective antagonists, d(CH2)5Tyr(Me)-[Orn8]vasotocin and Compound VI [d(CH2)5,Tyr(Me)2,Thr4,Tyr-NH2(9)]OVT (1 microgram/microliter), did not further increase their sodium intake. On the other hand, sodium appetite of sodium depleted female rats were inhibited by the same dose of pICV OT but not by the selective agonist Tyr4-Gly7 OT (1 microgram/microliter). The reduction od sodium appetite in female rats may have been in part due to the competitive behavior of grooming that followed the OT injection. Nevertheless, the OT inhibition in females of the need-free sodium intake and of the sodium appetite that occurs after furosemide but not in adrenalectomized or DOCA treated rats, argue for a mechanism independent from angiotensin or aldosterone alone related sodium appetite and the mechanism involved in the suppression of these salt intakes remain to be clarified.
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PMID:Sex difference in sensitivity to exogenous oxytocin in different models of sodium appetite in the rat. 859 19

Mesotocin is the oxytocin-like hormone found in most terrestrial vertebrates from lungfishes to marsupials, which includes all non-mammalian tetrapods (amphibians, reptiles, and birds). It has the largest distribution in vertebrates after vasotocin found in all non-mammalian vertebrates and isotocin identified in bony fishes. In this study, we report the cloning and functional characterization of the cDNA for the mesotocin receptor (MTR) from the urinary bladder of the toad Bufo marinus. The cloned cDNA encodes a polypeptide of 389 amino acids that shows the greatest similarity to the teleost fish isotocin receptor and to mammalian oxytocin receptors with mutations in extracellular loops which are involved in ligand binding. When expressed in COSM6 cells, MTR exhibits the following relative order of ligand affinity: mesotocin > vasotocin = oxytocin > vasopressin > hydrin 1, isotocin, hydrin 2. Injection of MTR cRNA into Xenopus laevis oocytes induces membrane chloride currents in response to mesotocin, which indicates the coupling of the mesotocin receptor to the inositol phosphate/calcium pathway. This response is inhibited by an oxytocin antagonist, but not by a vasopressin antagonist specific for V2 vasopressin receptors. MTR mRNA is not only found in toad urinary bladder, but also in kidney, muscle, and brain tissue of the toad as revealed by northern blot analysis and reverse-transcriptase PCR. The results suggest a variety of function for mesotocin and its receptor including, in particular, an involvement in the regulation of water and salt transport.
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PMID:Cloning and functional characterization of the amphibian mesotocin receptor, a member of the oxytocin/vasopressin receptor superfamily. 864 23

We have compared the expression patterns in transgenic mice of bovine oxytocin constructs consisting of the 0.9 kilobase pair (kbp) structural gene flanked by varying lengths of upstream and downstream sequences. Over 200 offspring were derived from fertilized one-cell mouse eggs injected with construct bOT6.5, which consists of 3 kbp of upstream sequences and 2.6 kbp of downstream sequences. However, no transgenic founders were identified. In parallel experiments with other constructs, 30% of pups carried integrated copies of the injected transgene DNA. It therefore appears that bOT6.5 is toxic to mouse embryos. As previously reported (Ang et al., 1991), bOT, consisting of 2.6 kbp of downstream sequences and 0.6 kbp of upstream sequences, was expressed in lung and in testicular Sertoli cells, but no expression was detected in the hypothalamus. bOT3.5, which consists of 0.6 kbp of upstream sequences and 1.9 kbp of downstream sequences, retains testis and lung expression, but, surprisingly, is also expressed in the hypothalamus. These data suggest that the 0.7 kbp of downstream sequences that are present in bOT, but which are absent from bOT3.5, contain elements that mediate the repression of hypothalamic expression. The activity of this repressor must be itself overcome in the normal genomic context of the bovine OT gene. Within the hypothalamus, in situ hybridisation analysis has revealed expression of bOT3.5 in the supraoptic nucleus (SON) and paraventricular nucleus (PVN), but not in the suprachiasmatic nucleus (SCN). In parallel with the response of the endogenous murine OT RNA, 7 days of salt-loading resulted in a significant increase in the level of transgene RNA in the SON. In the PVN, neither the endogenous OT RNA nor the transgene RNA responded significantly to salt-loading. Transgene RNA levels in the hypothalamus have also been shown to be elevated during late pregnancy and lactation.
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PMID:Oxytocin transgenic mice. 871 53

Plasma oxytocin (OT) levels are strongly correlated with inhibition of ingestion in many models of stimulated food and NaCl intake in rats, but peripheral administration of OT or OT antagonists has little or no effect on these behaviors. These findings led us to propose that central OT secretion from parvocellular neurons occurring in parallel with pituitary secretion from magnocellular neurons acts to inhibit ingestion of both food and salt. Multiple lines of evidence now support this hypothesis: 1) intracerebroventricular (icv) OT administration inhibits food intake in fasted rats and NaCl intake in hypovolemic rats; 2) icv administration of OT-receptor antagonists significantly blunts the effects of anorexigenic agents on food intake and the action of naloxone to inhibit hypovolemia-induced intake of NaCl, but not water; 3) most treatments that inhibit food and/or NaCl intake stimulate expression of c-fos in parvocellular as well as magnocellular OT neurons, indicating simultaneous activation of both centrally-projecting and pituitary-projecting OT neurons; 4) icv treatment with cytotoxic conjugates of ricin A and OT to disable cells bearing OT receptors leads to a disinhibition of NaCl intake similar to that produced by OT antagonists; 5) administration of ethanol, a well known inhibitor of OT secretion, produces effects on stimulated food and NaCl intake in rats analogous to those produced by OT-antagonists and ricin-OT conjugates. In conjunction with studies demonstrating natriuretic effects of circulating OT, these results therefore support the concept of coordinated central and peripheral OT secretion as a mechanism for regulating body solute homeostasis in rats. These phenomena will be used as a framework to discuss and critically evaluate the criteria that are both necessary and sufficient to firmly establish behavioral and physiological functions of centrally-secreted peptides such as OT.
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PMID:Establishing behavioral and physiological functions of central oxytocin: insights from studies of oxytocin and ingestive behaviors. 871 70

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