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

The contribution of oxytocin to the maintenance of renal Na+ excretion in the Brattleboro rat has been examined in animals infused with hypotonic saline. Brattleboro rats exhibited hypernatraemia and hyperosmolality associated with greatly increased plasma concentrations of oxytocin by comparison with Long-Evans control rats. Neurohypophysectomy to remove the secretion of the remaining posterior pituitary peptide, oxytocin, led to greatly diminished rates of Na+ excretion in the Brattleboro rat. Oxytocin replacement to achieve plasma levels equivalent to those in intact Brattleboro rats produced a substantial and sustained natriuresis in the neurohypophysectomized animal. Oxytocin secretion evoked in response to saline infusion would thus appear to be effective in promoting renal Na+ excretion in the absence of vasopressin in the Brattleboro rat.
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PMID:Influence of oxytocin on sodium excretion in the anaesthetized Brattleboro rat. 203 Mar 28

There are several medical methods of inducing 2nd trimester abortion, each with merits and drawbacks, difficult to compare, especially when supplemental techniques are used. Drugs used are hypertonic saline, urea, natural and synthetic prostaglandins (PGs), mannitol, formalin, ethacridine lactate (Rivanol) and others for intraamniotic route; saline, PGs, Rivanol, utus paste and other extraamniotically; and the above methods combined with oral antiprogestins, iv oxytocics, in or intravaginal PGs, or mechanical cervical dilators. Few double-blind studies exist comparing drugs. About 50,000 mid-trimester abortions are done in the US yearly, about 10% of all terminations, but these cause 2/3 of all complications and half of the deaths. Saline can be used after 15 weeks, can cause hypernatremia or coagulopathy, and takes up to 72 hours unless augmented with ocytocin and/or laminaria. Urea may have less risk of coagulopathy. Rivanol is considered safer than both in some countries, e.g., Scandinavia, Eastern Europe, Israel, India and Japan. It can be instilled transcervically. Various intrauterine PGs have been compared in several doses and routes by WHO Task Force research groups and others. Extraamniotic PGs require a lower dose, cause fewer cervical lacerations, and can be used when membranes are ruptured, in molar pregnancy, at Weeks 13-15, and in cases of fibroids. This route is somewhat less effective than intraamniotic PGs, and may require multiple doses. Intraamniotic PGs act slower but are more effective, after only 1 dose. Laminaria speed up the process, but adding oxytocin increases risk of injury. PGs may be safer than saline, especially if intramuscular route is used, because there is no danger of coagulation, cardiovascular, renal or hypernatremic complications or inadvertent injection. It is possible that some of the higher complications attributed to PGs are related to selection of patients with more severe medical conditions. PGs are more expensive, and require medication for side effects.
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PMID:Intrauterine administration of drugs for termination of pregnancy in the second trimester. 222 3

Regulation of posterior pituitary secretion of vasopressin (AVP) and oxytocin (OT) was studied in rats given electrolytic lesions of ventral nucleus medianus (vNM). As described previously, rats with such lesions were chronically hypernatremic and showed impaired drinking responses to an osmotic challenge. AVP secretion in response to osmotic stimuli also was significantly blunted, although sufficient increases in plasma AVP levels did occur, in association with an abnormally high range of plasma sodium concentrations, to allow urinary concentration comparable to control animals. These findings suggest that vNM lesions cause an upward resetting of the osmotic threshold for AVP secretion. In contrast, hypovolemia, produced by subcutaneous polyethylene glycol treatment, and hypotension, produced by phentolamine treatment, both evoked AVP responses in rats with vNM lesions that were equivalent to those seen in control animals. Plasma OT responses to osmotic and hemodynamic stimuli were analogous to the AVP responses. These findings reproduce the major clinical features observed in humans with the disorder of essential hypernatremia and by doing so support proposals that this disorder is caused by lesions in the vicinity of the anterior hypothalamus that result in selective destruction of afferent osmosensitive inputs to the neurohypophysis.
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PMID:Impaired secretion of vasopressin and oxytocin in rats after lesions of nucleus medianus. 407 88

An adolescent boy with essential hypernatremia, absent corpus callosum, mental retardation, hypodipsia, and partial diabetes insipidus with "inappropriate" ADH regulation and secretion was studied regarding factors controlling ADH and neurophysin release. Persistent hyperosmolality was noted while on 100 mEq sodium intake daily. Endogenous vasopressin activity was demonstrated after prolonged water deprivation. Hypertonic saline infusion produced increased volumes but dilute urine. Aqueous pitressin increased urinary osmolality, decreased serum osmolality, urine flow rate, and free water clearance. Stable water diuresis was induced by water loading and on normal saline infusion. Nicotine-stimulated neurophysin remained unexpectedly low and below the level of detectability when sampled during the physiologic studies, whereas oestrogen-stimulated neurophysin was elevated during oestrogen stimulation, water loading, and orthostasis procedures. Plasma vasopressin was suppressed with water loading but remained suppressed 90 min after tilt table testing. These data indicate impairment of the osmoreceptor mechanism: however, since the patient had a normal response of oestrogen-stimulated neurophysin, that part of the neurohypophysis appears intact. Chlorpropamide was effective in alleviating the hyperosmolar state acutely and maintained normal osmolar concentrations during two years of therapy.
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PMID:Essential hypernatraemia, antidiuretic hormone and neurophysin secretion: response to chlorpropamide. 746

Sustained hyperosmolality increases the levels of hypothalamic oxytocin (OT) and arginine vasopressin (AVP) messenger ribonucleic acids (mRNAs). Gonadectomy is known to abolish this response (12,18). In this study we investigated whether thyroidectomy would alter OT and AVP mRNA levels in the hypothalamic paraventricular nucleus (PVN) of the hyperosmotically stimulated rat. Male Sprague-Dawley rats underwent thyroidectomy (hypothyroid) or sham thyroidectomy (euthyroid) at 7 weeks of age. Three weeks later hypothyroid and euthyroid animals were administered 2% NaCl (6-11 days) or tap water and sacrificed at the end of the experiment. Northern blot hybridization was used to assess size and levels of hypothalamic OT and AVP mRNAs. Hypothyroid rats had significantly lower levels of serum thyroxine (T4) than their euthyroid cohorts (P < 0.0001). Both the euthyroid and the hypothyroid animals receiving 2% NaCl developed hypernatremia and increased the levels and the size of OT and AVP mRNAs compared to their tap water cohorts. We conclude that in contrast to gonadectomy, thyroidectomy does not alter the level of OT and AVP mRNAs in the hypothalamus of chronically hypernatremic male rats.
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PMID:Thyroidectomy does not alter hypothalamic oxytocin and vasopressin expression in chronically hypernatremic rats. 760 12

Sheep which were predominantly urinary excretors (U) or faecal excretors (F) of sodium were exposed to a 75% reduction of water intake for 72 h. The experiment was performed on moderate, low or high sodium intakes (0.4, 0.05 or 1.2 mmol kg-1 day-1) to test the hypothesis that dehydration natriuresis was not a cause of sodium depletion but a defence against hypernatraemia. Dehydration caused elevation of plasma sodium concentration, osmolality, antidiuretic hormone (ADH) and oxytocin but, as in other experiments, a fall in haematocrit. The two higher levels of sodium intake were associated with dehydration natriuresis but also a smaller increase in faecal sodium excretion in both U and F sheep. On low sodium intake, however, neither urinary nor faecal sodium excretion increased in either group of sheep although the rise in plasma sodium concentration caused by dehydration was similar. Thus, when there is a risk of sodium depletion, due to low sodium intake, dehydration natriuresis does not occur, consistent with the hypothesis. Active sodium transport inhibitor (ASTI) and atrial natriuretic peptide (ANP) fell rather than rose during dehydration. Since aldosterone is suppressed by the higher levels of sodium intake, none of these hormones is likely to mediate dehydration natriuresis in sheep. F sheep showed more effective renal and faecal water conservation when dehydrated. During water restriction, the urinary potassium excretion of U sheep was significantly reduced, unlike that of F sheep; moreover, the latter maintained an identical plasma potassium concentration between baseline and restriction period, whereas in U sheep it was 0.3 mmol l-1 higher during water restriction. Increased drinking rather than reduced urine output was the basis of rehydration when ad lib. water intake was restored.
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PMID:Responses to reduced water intake, including dehydration natriuresis, in sheep excreting sodium predominantly in urine or in faeces. 778 17

The effect of hypertonic NaCl consumption on vasopressin (VP) and oxytocin (OT) mRNA levels and plasma and pituitary peptides was evaluated in rats with sham or anterior ventral third ventricular (AV3V) lesions. Rats were given tap water or 2% NaCl for 4 days. Because the rats with lesions drank significantly less salt solution than the controls (78.8 +/- 17.4 vs. 205.5 +/- 37.8 ml/4 days), a second control group was included in which saline intake was matched to the lesioned group. AV3V rats showed a deficit in the peptide response to the osmotic stimulus. There was no increase in plasma VP or OT or decrease in posterior pituitary peptide content in the face of an extreme hypernatremia: plasma sodium of 180.1 +/- 4.2 meq/l. Evaluation of mRNA changes by means of in situ hybridization showed that animals with lesions responded to the salt challenge with increases in hypothalamic VP and OT mRNA levels. There were significant increases in paraventricular and supraoptic OT mRNA and paraventricular VP mRNA in the lesioned group. The salt-matched control group showed no changes in peptide mRNA levels. These results demonstrate that AV3V lesions produce an impairment of the salt-neuroendocrine reflex but a persistence of the peptide mRNA response. Differences in control mechanisms must account for this dissociation between peptide mRNA expression and peptide secretion.
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PMID:Dissociation between vasopressin and oxytocin mRNA and peptide secretion after AV3V lesions. 781 Jul 75

We investigated the modulatory role of gonadal steroids on the expression of oxytocin (OT) and vasopressin (AVP) cytoplasmic mRNAs in the paraventricular nucleus and supraoptic nucleus of the osmotically stimulated rat. We chronically administered an oral salt load (2% sodium chloride solution for 5 days) to intact and gonadectomized female and male Sprague-Dawley rats and measured serum sodium, body weight, pituitary content of OT and AVP immunoreactivities, and size and abundance of hypothalamic cytoplasmic OT and AVP mRNA transcripts. Intact and gonadectomized rats that were administered an osmotic challenge developed comparable degrees of hypernatremia and loss of body weight as well as depletion of posterior pituitary stores of OT and AVP. Hyperosmolality induced elongation of the OT and AVP transcripts in intact and gonadectomized animals, but only intact rats had enhanced hypothalamic cytoplasmic OT and AVP mRNA concentrations to this stimulus. Replacement with gonadal steroids restored the up-regulation in OT and AVP gene expression in gonadectomized animals rendered hyperosmolar. The findings support a modulatory role for gonadal steroids in hypothalamic OT and AVP gene expression during osmotic stimulation.
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PMID:Gonadal steroid modulation of oxytocin and vasopressin gene expression in the hypothalamus of the osmotically stimulated rat. 824 94

In a previous study in rats we demonstrated the existence of osmoregulatory natriuretic mechanisms distinct from the natriuretic mechanisms that are dependent on volume stimulation. At the same time, we found that oxytocin (OT) receptors were important mediators of natriuresis induced by hypernatremia but not of that induced by isotonic volume expansion. In the present study, the role of OT in dehydration natriuresis was examined in conscious rats. Dehydration for 24 h caused hypernatremia (from 142.1 +/- 0.4 to 147.7 +/- 0.7 mmol/l) and natriuresis accompanied by an approximately 30% spontaneous reduction of food intake. In conjunction with renal retention of water caused by an increase in circulating vasopressin, the natriuresis and probably the reduction of food intake can help to counteract the rise in body fluid osmolality. This natriuresis could not be fully explained by the reduction in plasma aldosterone. Plasma OT concentration had increased from 15.5 +/- 1.2 to 23.8 +/- 2.0 pg/ml at the end of 24 h of dehydration. Intravenous infusion of a selective OT-receptor antagonist [Mpa1,D-Tyr(Et)2, Thr4, Orn8]-OT using osmotic minipumps prevented dehydration natriuresis. It is concluded that in a dehydration-induced hypernatremic state OT is released, inducing natriuresis and facilitating sodium homeostasis. This mechanism is activated by Na osmoreceptors, but is not primarily dependent on the volume status.
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PMID:Dehydration natriuresis in male rats is mediated by oxytocin. 877 75

Centrally-mediated responses to plasma hyperosmolality include compensatory drinking and pituitary secretion of vasopressin and oxytocin in both adult and neonatal rats. However, the anorexia that is produced by plasma hyperosmolality in adult rats is not evident in neonates, perhaps due to functional immaturity of osmoresponsive hindbrain circuits. To examine this possibility, the present study compared treatment-induced brain expression of the immediate-early gene product c-Fos as a marker of neural activation in adult and two-day-old rats after subcutaneous injection of 2 M NaCl (0.1 ml/10 g body weight). This treatment produced marked hypernatremia in adult and two-day-old rats without altering plasma volume. Several brain regions (including components of the lamina terminalis, the paraventricular and supraoptic nuclei of the hypothalamus, and the area postrema) were activated to express c-Fos similarly in adult and two-day-old rats after 2 M NaCl injection, consistent with previous reports implicating a subset of these regions in osmotically-stimulated drinking and neurohypophyseal secretion. In contrast, other areas of the brain that were activated to express c-Fos in adult rats after 2 M NaCl injection were not activated in neonates: these areas included the central nucleus of the amygdala, the parabrachial nucleus and catecholamine cell groups within the caudal medulla. This study demonstrates that certain brain regions that are osmoresponsive in adult rats (as defined by induced c-Fos expression) are not osmoresponsive in two-day-old rats. When considered in the context of known differences between the osmoregulatory capacities of adult and neonatal rats, our results are consistent with the idea that osmoresponsive forebrain centres are primarily involved in osmotically-stimulated compensatory drinking and neurohypophyseal secretion, whereas osmoresponsive regions of the hindbrain are important for concomitant inhibition of feeding and gastric emptying.
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PMID:Central c-Fos expression in neonatal and adult rats after subcutaneous injection of hypertonic saline. 921 75


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