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

The effects of PGI-salt and PGI-2 methyl ester on intrauterine pressure (IUP) and uterine electromyographic activity (EMG) were examined in vivo in non-pregnant ovariectomized sheep. PGI-2 salt and PGI-2 methyl ester (50--200 micrograms) reduced significantly the frequency and amplitude of IUP cycles and also inhibited the associated uterine EMG activity. Injections of oxytocin (50 mU) or PGF-2 alpha (2 micrograms) partly overcame the inhibiton of IUP induced by the PGI-2 methyl ester. These results suggest that endogenous PGI-2 may be involved in the regulation of uterine activity in sheep.
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PMID:Inhibition by PGI-2 of myometrial activity in vivo in non-pregnant ovariectomized sheep. 675 Jan 8

The binding to bovine neurophysin of lysine-vasopressin and of lysine-vasopressin selectively deuterated at the protons ortho to the tyrosine hydroxyl was studied by proton n.m.r. and equilibrium dialysis. The principal object of these studies was to investigate reports that, at standard salt concentrations, neurophysin contained a second site specific for vasopressin. At pH 6, the effects of neurophysin-I on the line-width, longitudinal relaxation rate and nuclear Overhauser properties of the lysine-vasopressin tyrosine ring protons were interpretable in terms of a slow-exchange 1:1 interaction between lysine-vasopressin and neurophysin. Additionally, n.m.r. competition studies between lysine-vasopressin and L-phenylalanyl-L tyrosinamide suggested 1:1 competition for a single binding site on neurophysin. No evidence pointing to a significant second lysine-vasopressin-binding site was obtained from the n.m.r. studies. The lack of a moderately strong second binding site for lysine-vasopressin at neutral pH was also indicated by equilibrium dialysis studies at relatively high free hormone concentrations. These studies demonstrated only a single thermodynamically significant site for either oxytocin or vasopressin and failed to confirm a reported effect of LiCl on the number of sites available to oxytocin. It is suggested that secondary sites for the hormones are probably markedly weaker and less specific than reported elsewhere.
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PMID:N.M.R. and equilibrium dialysis studies of the interaction of bovine neurophysin-1 with vasopressin and small peptides. 721 20

1. The present study investigates the nature and magnitude of the renal response to plasma levels of oxytocin which might be induced by salt loading. 2. Increased plasma osmolality induced by loading with NaCl is an effective stimulus for oxytocin release in the unanaesthetized male rat. Plasma oxytocin concentration was positively correlated (r = 0-.77) with plasma osmolality. Plasma oxytocin (muu./ml.) = 0.37 x (plasma osmolality (m-osmole/kg) -297). 3. In anaesthetized Long Evans rats intra-atrial administration of oxytocin at rates of 0.05 and 0.15 m-u./ml. produced plasma hormone concentrations (5 +/- 1 and 16 +/- 2 mum./ml. respectively) within the range induced by salt loading. 4. Oxytocin administration at 0.15 and 1.5 m-u./min in Long Evans rats produced dose-related increases in urine flow and Na+ and Cl- excretion. Renal responses to 0.05 m-u. oxytocin/min were equivocal. 5. Oxytocin administration at 0.15 m-u./min was ineffective in Brattleboro rats but 1.5 m-u./min led to increased Na+ and Cl- excretion and a reduction in urine flow. 6. Plasma oxytocin levels similar to those induced by severe dehydration or salt loading are effective in increasing renal Na+ and Cl- excretion and urine flow. These effects on water and electrolyte excretion appear to be independent of each other and both may be modified by the presence or absence of vasopressin. 7. This study provides no evidence for a major role for oxytocin in the day to day regulation of salt or water balance under conditions of normal hydration in the male rat.
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PMID:Release of oxytocin induced by salt loading and its influence on renal excretion in the male rat. 723 26

Chronic salt loading up-regulated the expression of neuronal nitric oxide synthase (NOS) mRNA in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus with a concomitant increase in NOS activity in the posterior pituitary. Once daily ip injection of N-omega-nitroarginine (N-Arg), a NOS inhibitor, significantly inhibited NOS activity in the posterior pituitary in a dose-dependent manner, but did not influence NOS mRNA levels. Two percent salt loading for 3 or 4 days significantly depleted the contents of both arginine vasopressin (AVP) and oxytocin (OT) in the posterior pituitary, and simultaneous treatment with daily injections of N-Arg at a dose of 10 mg/kg significantly enhanced the depletion of both AVP and OT. This effect was dose dependent and paralleled the inhibition of NOS activity in the posterior pituitary. N-Arg treatment had no effect on the levels of both AVP and OT transcripts in PVN or SON. These results suggest that NOS gene expression in the SON and PVN of the rat hypothalamus is increased during hyperosmotic stimulation and suggest a neuromodulatory role for NO in the rat hypothalamo-hypophysial system as an inhibitory regulator of AVP and OT secretion.
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PMID:Up-regulation of nitric oxide synthase (NOS) gene expression together with NOS activity in the rat hypothalamo-hypophysial system after chronic salt loading: evidence of a neuromodulatory role of nitric oxide in arginine vasopressin and oxytocin secretion. 750 33

Magnocellular hypothalamic neurons of the paraventricular (PVN) and supraoptic (SON) nuclei have been shown to contain a wide variety of messenger molecules in addition to vasopressin and oxytocin, including the nitric oxide (NO)-synthesizing enzyme (NOS). In this paper we have investigated the effects of salt loading on the expression of NOS by means of immunohistochemistry and in-situ hybridization. The results show an increase in the number of NOS-immunoreactive (IR) neurons both in the PVN and the SON after 5 and 14 days of salt loading. Several of these neurons were double labelled with vasopressin antiserum. In situ hybridization showed a marked increase in the number of neurons expressing NOS mRNA and a stronger signal in individual neurons. The present results suggest a role for NO in the magnocellular hypothalamic system after salt loading.
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PMID:Nitric oxide synthase increases in hypothalamic magnocellular neurons after salt loading in the rat. An immunohistochemical and in situ hybridization study. 751 26

These studies evaluated the involvement of central oxytocin (OT) and atrial natriuretic peptide (ANP) receptors in the osmotic inhibition of hypovolemia-induced salt appetite. Rats were pretreated centrally with the A chain of the cytotoxin ricin conjugated to OT (rAOT) or ANP (rAANP) to selectively inactivate cells bearing these respective receptors, or rats were pretreated with the unconjugated A chain (rA) as a control. Hypovolemia was induced with subcutaneous colloid injections, and rats then were given either 2 M mannitol, which raises plasma osmolality but lowers plasma sodium, or 1 M NaCl, which raises both. Hypertonic mannitol inhibited saline ingestion in rA-treated control rats but stimulated ingestion in rAOT- and rAANP-treated rats, whereas hypertonic NaCl blunted saline ingestion in rA- and rAOT-treated rats but stimulated ingestion in rAANP-treated rats. Angiotensin II-induced saline intake was similarly potentiated in rAOT- and rAANP-treated rats, indicating that this treatment also activates central inhibitory OT and ANP pathways. These data suggest that central ANP receptors mediate both Na(+)- and osmolality-induced inhibition of NaCl ingestion, whereas central OT receptors primarily mediate osmolality-induced inhibition of NaCl ingestion in rats.
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PMID:Central oxytocin and ANP receptors mediate osmotic inhibition of salt appetite in rats. 765 44

Rats drinking ad libitum tap water or hypertonic (i.e. 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.), for three days, thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with TRH resulted in significantly decreased hypothalamic oxytocin content in both euhydrated (i.e. given tap water ad libitum) and salt-loaded rats. In rats drinking tap water, neurohypophysial oxytocin content decreased. Plasma oxytocin concentration was distinctly elevated under TRH treatment in rats euhydrated but, on the contrary, decreased in salt-loaded rats as compared with animals similarly drinking hypertonic saline but not TRH-treated. The present data suggest that TRH may be involved in some regulatory processes related to oxytocin biosynthesis and release from the rat hypothalamo-neurohypophysial system.
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PMID:Thyrotropin-releasing hormone (TRH) modifies oxytocin release from the hypothalamo-neurohypophysial system in salt-loaded rats. 767 Jan 25

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

Magnocellular neurons of the supraoptic (SON) and paraventricular (PVN) nuclei projecting to the neurohypophysis produce, in addition to the classical hormones vasopressin and oxytocin, a large number of other peptides, one of which is cholecystokinin (CCK). Binding sites for CCK have been identified in the posterior pituitary. Recently the cDNAs for CCKA and CCKB receptors were isolated and characterized, and CCKA and CCKB receptor mRNAs were localized in the SON and PVN. We have used complementary oligonucleotides and in situ hybridization histochemistry to study CCKB receptor mRNA in hypothalamic neurons. Changes in the expression of CCKB receptor mRNA in the SON and PVN were analysed in salt-loaded as well as in hypophysectomized animals. Levels of CCKB receptor mRNA in the PVN and SON increased markedly in salt-loaded animals as compared to controls. An increase in CCKB receptor mRNA levels was seen in the SON and PVN after 3 days of salt loading, with high levels continuing through 5 and 7 days. At 14 days, the levels of CCKB receptor mRNA in the PVN were significantly lower as compared to 7 days. Hypophysectomy 5 days prior to sacrifice, resulting in a nerve lesion in the neurohypophysial pathway and removal of the anterior pituitary hormones, induced a significant increase in CCKB receptor mRNA levels in neurons of the PVN. The increase in CCKB receptor mRNA labelling after salt loading was mainly observed in the ventrolateral part of the PVN and in the dorsolateral part of the SON, corresponding to oxytocin-containing neurons, whereas the increase after hypophysectomy was mainly seen in the central part of the PVN and in the ventral part of the SON, corresponding to vasopressin-containing neurons. The results suggest that the synthesis of CCKB receptors in magnocellular neurons is increased upon osmotic challenge and hypophysectomy.
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PMID:Cholecystokinin B receptor gene expression in hypothalamic neurosecretory neurons after experimental manipulations. 784 36

Mammals have evolved sophisticated behavioral and physiological responses to oppose changes in the osmolality of their extracellular fluid. The behavioral approach consists of regulating the intake of salt and water through changes in sodium appetite and thirst. The physiological approach comprises adjustments of renal excretion of water and sodium which are achieved through changes in the release of antidiuretic and natriuretic hormones. Individually, these osmoregulatory responses are controlled by "osmoreceptors": groups of specialized nerve cells capable of transducing changes in external osmotic pressure into meaningful electrical signals. Some of these sensors are located in the region of the hepatic portal vein, a strategic site allowing early detection of the osmotic impact of ingested foods and fluids. Changes in systemic osmolality, however, are detected centrally, within regions that include the medial preoptic area, the median preoptic nucleus, the organum vasculosum lamina terminalis (OVLT), the subfornical organ, and the supraoptic nucleus (SON). While studies have indicated that these central and peripheral osmoreceptors participate in the control of osmoregulatory responses, little is known of the mechanisms by which this is achieved. One notable exception, however, consists of the osmotic control of electrical activity in SON neurons which, in the rat, contributes to the regulation of natriuresis and diuresis through effects on the secretion of oxytocin and vasopressin. Previous studies have shown that these cells are respectively excited and inhibited by hypertonic and hypotonic conditions. Experiments in vitro indicate that these responses result from both the endogenous osmosensitivity of these cells and changes in synaptic drive. Patch-clamp analysis has revealed that SON neurons are respectively depolarized and hyperpolarized by increases and decreases in external osmolality and that these intrinsic responses result from changes in the activity of mechanosensitive cationic channels. Moreover, intracellular recordings in hypothalamic explants have shown that changes in electrical activity are associated with proportional changes in the frequency of glutamatergic excitatory postsynaptic potentials derived from osmosensitive OVLT neurons. Both of these mechanisms, therefore, may participate in the osmotic regulation of neurohypophysial hormone release in situ.
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PMID:Osmoreceptors, osmoreception, and osmoregulation. 785 14


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