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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 oxytocin, a uterotonic polypeptide hormone, on the voltage-dependent slow calcium, fast sodium, and potassium channel currents were studied using whole-cell voltage clamp of freshly isolated cells from late pregnant (18-21 day) rat myometrium. The calcium current was rapidly inhibited by oxytocin (about 25% inhibition at 20 nM) in a dose-dependent manner, and this inhibitory effect was completely reversible by washout. However, inhibition was not observed when barium was used as the charge carrier. Sodium current and potassium current were not modified by oxytocin, thus sodium and potassium currents may not play important roles in oxytocin-induced augmentation of uterine contraction. It is concluded that oxytocin stimulates uterine contraction by mechanisms other than augmentation of the voltage-dependent calcium current, e.g., by release of Ca from sarcoplasmic reticulum (by inositol triphosphate) or by activation of a receptor-operated Ca channel. The inhibition of the slow calcium current may be induced by the elevation of [Ca]i.
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PMID:Oxytocin actions on voltage-dependent ionic channels in pregnant rat uterine smooth muscle cells. 128 86

Seventy pregnant Nigerian women requiring oxytocin for the induction or augmentation of labour were randomized into two groups, one administered 5% glucose, and the other 0.9% saline as vehicle for oxytocin. Another group of seventy women who did not receive intravenous fluids in labour were included for comparison. Sodium ion concentration in maternal antepartum and postpartum plasma as well as umbilical cord plasma samples were estimated in all the patients. There was a statistically significant fall in the maternal postpartum plasma sodium concentration relative to the ante-partum values only in patients receiving 9% glucose solution (P less than 0.001). There was also a significant correlation between the sodium levels in maternal postpartum and cord plasma samples, suggesting that these changes were transmitted to the fetus transplacentally. The use of normal saline as a vehicle for oxytocin administration in parturient women can prevent the hyponatraemia associated with the use of 5% glucose for this purpose.
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PMID:Effects of using either saline or glucose as a vehicle for infusion in labour. 204 Feb 41

Synapses in the lateral septum of the murine brain have been investigated by ultrastructural immunocytochemistry, using monoclonal anti-neurophysins in both immunoperoxidase and immunogold techniques. In the region shown by light microscopy to be rich in vasopressinergic innervation, synaptic boutons containing approximately 30 nm clear vesicles and occasional approximately 100 nm dense-cored granules (granules) were stained by pre-embedding immunoperoxidase procedures with antisera to vasopressin-neurophysin, but not oxytocin-neurophysin; reaction product was diffusely distributed in the terminals. Terminals were symmetrical, and both axosomatic and axodendritic in type. Postembedding immunogold procedures by use of anti-vasopressin-neurophysin labeled only the approximately 100 nm diameter granules in the terminals. Sodium meta-periodate treatment 'bleached' immunoreactive granules, indicating the presence of a carbohydrate residue. The quantum of peptide packaged in the granules appears to be smaller than that in magnocellular neurones; nevertheless, the results indicate that, as in the magnocellular neurosecretory system, vasopressin and its neurophysin are packaged exclusively in granules, and that vasopressin in the septum is likely to be derived from a precursor comprising vasopressin, vasopressin-neurophysin and a glycosylated residue.
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PMID:Ultrastructural characterisation of vasopressinergic terminals in the lateral septum of murine brains by use of monoclonal anti-neurophysins. 330 50

Plasma samples obtained at 4-h intervals from goats for at least 24 h before and then during 24 h of deprivation of water were analysed by radioimmunoassay for vasopressin and oxytocin concentrations. The samples were also analysed for osmolality and sodium concentration. The differential effect of night/day versus day/night deprivation was also studied. During the two periods before the two deprivations osmolality varied in a regular manner, with low values occurring at 08.00 h. Sodium concentration followed osmolality, whereas vasopressin did not vary during the period before deprivation. During deprivation vasopressin increased along with osmolality and sodium concentration, with the beginning of the increase occurring after the morning feed. Oxytocin levels did not increase during the period of deprivation. These results do not support the hypothesis of general release of neurohypophysial hormones in response to osmotic stimuli but instead indicate there are species variations with respect to hormonal response to water deprivation.
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PMID:Vasopressin, but not oxytocin, is released in response to water deprivation in conscious goats. 374 67

Imidazole (3.67 x 10(-3) M) and sodium bicarbonate (1.78 x 10(-2) M) failed to alter acetylcholine evoked responses in isolated rat uterus but they produced a significant shift of the log dose-response curve of oxytocin to the left. This potentiating effect was reversible. Addition of imidazole increased the pH of de Jalon solution from 7.2 to 8.5. Sodium dihydrogen orthophosphate (3.3 x 10(-3) M) prevented the change of pH due to the addition of imidazole and at the same time the potentiating effect of imidazole was inhibited. The present study strongly suggests that the potentiation of oxytocin-evoked responses by imidazole is due to the change in pH of de Jalon solution towards more alkaline range and it may not be due to stimulation of phosphodiesterase activity of rat uterus.
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PMID:Effect of imidazole on oxytocin and acetylcholine induced responses in isolated rat uterus: with observations on its mechanism of action. 743 34

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

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

Fos immunoreactivity was used to map the neuronal population groups activated after sodium ingestion induced by peritoneal dialysis (PD) in rats. Oxytocin immunoreactivity in combination with Fos immunoreactivity was also analyzed to evaluate whether the oxytocinergic neurons of the paraventricular nucleus of the hypothalamus (PVN) are activated during the satiety process of sodium appetite. Sodium ingestion stimulated by PD produced Fos immunoreactivity within defined cells groups of the lamina terminalis and hindbrain areas such us the nucleus of the solitary tract, area postrema, and lateral parabrachial nucleus. On the other hand, particular parvocellular and magnocellular oxytocinergic subdivisions of the PVN and supraoptic nucleus were double labeled after PD-induced sodium consumption. Approximately 27 and 2.1%, respectively, of the activated dorsomedial cap and parvocellular posterior subnuclei of the PVN, which project to the hindbrain, were oxytocinergic. Our data indicate that specific neuronal groups are activated during the satiety process of sodium appetite, suggesting they may form a circuit subserving sodium balance regulation. They also support a functional role for the oxytocinergic neurons in this circuit.
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PMID:Distribution of Fos immunoreactivity in rat brain after sodium consumption induced by peritoneal dialysis. 1019 1

Parallel and antiparallel heterodimers have been synthesized that combine into a single molecule the neurohypophyseal hormone oxytocin and the potent vasopressin V(2)-antagonist d(CH(2))(5)[D-Ile(2), Ile(4)]arginine vasopressin. Solid-phase synthesis with N(alpha)-9-fluorenylmethyloxycarbonyl (Fmoc) chemistry, featuring appropriate combinations of orthogonal protecting groups for the thiols [S-(N-methyl-N-phenylcarbamoyl)sulfenyl (Snm); S-acetamidomethyl (Acm); S-triphenylmethyl (Trt)], was used to assemble the required linear nonapeptide amide monomer intermediates, which were then brought together in defined ways by solution reactions to provide the two heterodimers. The first disulfide bridge was formed by a directed approach involving attack by the free thiol of the 1-beta-mercapto-beta, beta-cyclopentamethylenepropionic acid (Pmp) residue of one monomer onto the Snm group of a cysteine residue on the other monomer; the inverse directed strategy failed due to steric hindrance. The second disulfide bridge was formed by iodine co-oxidation of Cys(Acm) residues on adjacent chains. Biological studies revealed that both the parallel and antiparallel chimeras lack pressor activity, have low uterotonic activity, and have diuretic activities comparable to that of the monomeric V(2)-antagonist. Sodium excretion depends on experimental conditions. Thus, with a 4% water load, both chimeras display effects similar to that of an equimolar mixture of oxytocin and V(2)-antagonist, i.e., lower sodium excretion than that resulting from administration of oxytocin alone but higher than that when V(2)-antagonist was administered alone. However, when no water load was used, the parallel chimera proved to be more effective in promoting sodium excretion than either oxytocin alone or an equimolar mixture of oxytocin and V(2)-antagonist.
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PMID:Chemical syntheses and biological studies on dimeric chimeras of oxytocin and the V(2)-antagonist, d(CH(2))(5)[D-Ile(2), Ile(4)]arginine vasopressin. 1058 9

This study evaluates the relative importance of several mechanisms possibly involved in the natriuresis elicited by slow sodium loading, i.e. the renin-angiotensin-aldosterone system (RAAS), mean arterial blood pressure (MAP), glomerular filtration rate (GFR), atrial natriuretic peptide (ANP), oxytocin and nitric oxide (NO). Eight seated subjects on standardised sodium intake (30 mmol NaCl day(-1)) received isotonic saline intravenously (NaLoading: 20 micromol Na(+) kg(-1) min(-1) or approximately 11 ml min(-1) for 240 min). NaLoading did not change MAP or GFR (by clearance of (51)Cr-EDTA). Significant natriuresis occurred within 1 h (from 9 +/- 3 to 13 +/- 2 micromol min(-1)). A 6-fold increase was found during the last hour of infusion as plasma renin activity, angiotensin II (ANGII) and aldosterone decreased markedly. Sodium excretion continued to increase after NaLoading. During NaLoading, plasma renin activity and ANGII were linearly related (R = 0.997) as were ANGII and aldosterone (R = 0.999). The slopes were 0.40 pM ANGII (mi.u. renin activity)(-1) and 22 pM aldosterone (pM ANGII)(-1). Plasma ANP and oxytocin remained unchanged, as did the urinary excretion rates of cGMP and NO metabolites (NO(x)). In conclusion, sodium excretion may increase 7-fold without changes in MAP, GFR, plasma ANP, plasma oxytocin, and cGMP- and NO(x) excretion, but concomitant with marked decreases in circulating RAAS components. The immediate renal response to sodium excess appears to be fading of ANGII-mediated tubular sodium reabsorption. Subsequently the decrease in aldosterone may become important.
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PMID:Mechanisms of acute natriuresis in normal humans on low sodium diet. 1252 45


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