Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Slices from ox neurohypophyses were incubated in a calcium-free medium with the ionophores A23187 or X537A. X537A (5 X 10(-5) mol/l) caused a marked release of vasopressin, neurophysin and protein to the medium. A23187 (2 X 10(-5) mol/l) did not cause any release by itself, but when Ca2+ was added to the medium in the presence of the ionophore, an increase in the release of vasopressin, neuorphysin and protein occurred. Release of lactate dehydrogenase and peptidase were not affected by the ionophores. The secretion caused by A23187 was abolished by D600 (a verapamil analogue) (2 X 10(-5) mol/l) whereas the effect of X537A was unchanged. The effects of X537A were strongly inhibited by removal of sodium from the medium. Re-addition of sodium to the medium caused a marked release. Gramicidin (10(-6) or 5 X 10(-5) mol/l) had no effect on secretion. Efflux of 45Ca2+ from pre-loaded slices was drastically reduced in a sodium-free medium. X537A caused an increase in the efflux rate of 45Ca2+ both in medium with a normal concentration of sodium and when slices had been incubated in a sodium-free medium. A23187 and X537A both released 45Ca2+ from a neurohypophyseal mitochondrial fraction. When sodium in a concentration of 20 mmol/l was added to this fraction, the Ca2+ accumulation was inhibited. This effect was reduced by inorganic phosphate up to a concentration of 2 mmol/l.
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PMID:Calcium and stimulus secretion coupling in the neurohypophysis. V. The effects of the Ca2+ ionophores A23187 and X537 A on vasopressin release and 45Ca2+ efflux; interactions with sodium and a verapamil analogue (D600). 6 Aug 66

1. A-V differences and milk concentrations of respiratory gases, pH, HCO3 and H2CO3 have been measured in lactating goats and cows. 2. The pH and [HCO3 minus] of milk were significantly lower than those of plasma while milk PCO2 was virtually identical to that of mammary venous blood. [H2CO3+ dissolved CO2] was similar in milk and blood. 3. 14-C (from injected [14-C]HCO3 minus was found to cross the mammary epithelium in both directions. 14-C also passed across the duct epithelium and since this epithelium has previously been shown to be impermeable to ions it is argued that 14-C crossed in an unionized form, i.e. as CO2 and/or H2CO3. 4. Hourly milking with the aid of oxytocin raised milk pH, [HCO3 minus], [H2CO3], [Na] and E1Cl], and lowered [K], [lactose] and [phosphate]. These effects are discussed in relation to the hypothesis proposed previously for the action of oxytocin on milk composition. 5. A scheme for the distribution and movements of CO2, H2CO3 and HCO3 minus between extracellular fluid and milk is suggested, and discussed in relation to Cl minus transport.
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PMID:The distribution and movements of carbon dioxide, carbonic acid and bicarbonate between blood and milk in the goat. 23 18

1. The time course of appearance of radioactivity in milk was studied following close-arterial infusion of labelled phosphate, Ca or leucine into the mammary artery of lactating goats. Maximum activities were reached at 1.5 hr in all milk fractions including inorganic soluble phosphate, inorganic colloidal phosphate, casein P, soluble Ca, protein-associated Ca and casein. 2. At 0.5 hr, labelling of the soluble and colloidal phosphate fractions was significantly higher than that of the casein P. 3. Recovery of 32P or 47Ca 3 or more hours after infusion into the cistern of the mammary glands was 98% or greater, indicating that the mammary epithelium is virtually impermeable to [32P]phosphate and 47Ca in the milk to blood direction. 4. Ca and P failed to enter milk in excess of the normal secretion rate when the milk was diluted with isosmotic sucrose given by intraductal injection. 5. These data suggest that milk Ca and phosphate in their various forms are secreted, like protein and lactose, by exocytosis of Golgi vesicles. Unless a paracellular pathway is present, as in oxytocin-treated animals, the milk concentrations are maintained by virtue of the impermeability of the mammary epithelium to these substances.
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PMID:The secretion of calcium and phosphorus into milk. 46 1

It has been shown by surface potential measurements that lysine vasopressin and oxytocin may be bound by ionic surfaces to very varied extents. To dodecyl sulphate and phosphatidylserine monolayers the binding is very strong and is comparable to that for biological receptors such as those in toad bladder. For dioleyl phosphate and the carboxyl group of the polypeptide alamethicin, the binding is rather weaker while, for the zwitterionic lipids phosphatidylcholine and phosphatidylethanolamine, and for the erythrocyte surface, which contains two varieties of carboxylic acid group, no interaction seems to take place. In no system does the lysyl amino group of the vasopressin appear necessary for adsorption and, in the dodecyl sulphate monolayers, the interaction is strong even when the ionization of the terminal alpha-amino group is suppressed.
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PMID:The adsorption of lysine vasopressin at ionized interfaces. 98 72

1. Vaginal dilatation for 30 seconds caused a rapid and brief increase in intramammary pressure which was equivalent to that evoked by 160 muU of oxytocin (Syntocinon) injected intravenously. 2. The rise in mammary pressure induced by the stimulation of the central end of a severed vagus nerve for 30 seconds (5 V, 0,5 ms, 50 HZ) was similar to the response obtained with an intravenous injection of 360 muU of oxytocin. 3. The vago-pituitary reflex leads to the liberation of large amounts of antidiuretic hormone which does not interfere with the effect of oxytocin on the mammary gland, since dexamethasone phosphate prevented the vasopressor effect without significantly affecting the increase in intramammary pressure.
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PMID:[Level of oxytocin release induced by vaginal dilatation (Ferguson reflex) and vagal stimulation (vago-pituitary reflex) in lactating rats (author's transl)]. 120 94

The interaction of oxytocin with bovine neurophysin II in 0.1 M-sodium phosphate, pH 5.8, was investigated by equilibrium-dialysis and sedimentation studies. Sigmoidality of the binding curve is attributed to isomerization, either hormone-induced or pre-existing, with preferential binding of oxytocin to one isomeric state. Results are consistent with a binding equation of the form r = (2P[S]+2PQ[S]2)/(1+2P[S]+PQ[S]2) and values of 0.7 X 10(5)M-1 and 1.3 X 10(5)M-1 for P and Q respectively. The significance of these two parameters in relation to current theories of allostery is also discussed.
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PMID:Co-operative binding of oxytocin to bovine neurophysin II. 123 94

This study was conducted to determine whether platelet-activating factor (PAF) (1) attenuated oxytocin-induced secretion of the prostaglandin (PG) F2 alpha metabolite, PGFM, by the ovine uterus in situ and (2) inhibited the generation of the inositol phosphate secondary messengers by endometrial tissue in response to oxytocin challenge in vitro. Ovariectomized ewes received steroid replacement to mimic the luteal phase. Six ewes received intrauterine injections of 200 micrograms PAF/uterine horn/day on Days 11-15, and 6 ewes were treated with vehicle. All ewes received 1 microgram oxytocin i.v. on Days 13-16. Pretreatment of ewes with PAF significantly suppressed PGFM release in response to oxytocin on Days 14 and 15 (p less than 0.005) compared to vehicle-treated ewes. PAF was not administered on Day 16, and the PGFM response to oxytocin was not different between groups. In a second experiment, ewes were given intrauterine injections of 200 micrograms PAF/uterine horn/day (n = 8) or vehicle (n = 7) on Days 11-15, and all ewes received 1 microgram oxytocin i.v. on Days 13 and 14. On Day 15 the uterus was removed, and the incorporation of 3H-inositol into inositol phosphates was determined in caruncular endometrium. Treatment of ewes with PAF in vivo reduced inositol monophosphate (IP1) generated by oxytocin (10(-6) M) by 56.4%, compared to that in endometrium from vehicle-treated controls, and also inhibited the incorporation of 3H-inositol into glycerophosphoinositol (GPI). If PAF was added to the endometrium during the incubation in vitro, the attenuation of inositol phosphate generation did not occur.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that platelet-activating factor suppresses uterine oxytocin-induced 13,14-dihydro-15-keto-prostaglandin F2 alpha release and phosphatidylinositol hydrolysis in the ewe. 139 26

This study examined the effects of progesterone and intrauterine injection of ovine conceptus secretory proteins (oCSP) on endometrial responsiveness to oxytocin. Twelve ewes were ovariectomized on day 4 of the cycle (oestrus = day 0) and assigned in a 2 x 2 factorial arrangement, to receive either 1.5 mg ovine serum proteins (SP) or oCSP containing 25 micrograms ovine trophoblast protein 1 (oTP-1) (by radioimmunoassay) in 1.5 mg total protein into each uterine horn, via catheters, twice a day on days 11, 12, 13 and 14. Ewes received 200 mg progesterone per day (i.m.) from day 4 to day 10 or 15. Oxytocin-induced prostaglandin F2 alpha was measured as 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) on days 11, 12, 13 and 14 in plasma from three integrated, 10 min (10 ml) blood samples (0-10, 10-20, 20-30 min) obtained after intravenous injection of 20 iu oxytocin, and in a pre-oxytocin (-10 to 0 min) sample collected via an indwelling jugular catheter. The pre-oxytocin samples were also assayed for progesterone. Oxytocin-induced turnover of inositol phosphate was determined in endometrium on day 15 after hysterectomy. In ewes receiving progesterone to day 10, plasma progesterone decreased from about 12 to 2 ng ml-1 (SEM +/- 2.6) during the treatment period (days 11-14), but remained high (12-20 +/- 2.6 ng ml-1) in ewes that received progesterone to day 15. Intrauterine injection of oCSP resulted in high basal concentrations of PGFM on days 12 and 13 compared with SP-treated ewes (P less than 0.01). Treatments with progesterone did not affect basal PGFM concentrations. Treatment with oCSP abolished oxytocin-induced endometrial secretion of prostaglandin only if progesterone was maintained to day 15 (P less than 0.01); in ewes receiving such treatment, oCSP inhibited (P less than 0.01), but SP did not inhibit, oxytocin-induced endometrial turnover of inositol phosphate (P less than 0.06), which was greater in ewes treated with progesterone to day 10 than in those treated to day 15 (P less than 0.05). Ewes that responded to oxytocin with increased PGFM exhibited increased oxytocin-stimulated turnover of inositol phosphate on day 15. These results indicate that the antiluteolytic action oTP-1 exerts on the endometrium requires progesterone and that this mechanism involves inhibition of oxytocin-stimulated turnover of inositol phosphate.
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PMID:Effects of ovine conceptus secretory proteins and progesterone on oxytocin-stimulated endometrial production of prostaglandin and turnover of inositol phosphate in ovariectomized ewes. 162 35

Earlier studies have shown that lactation-induced bone loss in the rat is both PTH- and vitamin D-independent and have suggested the involvement of another, as yet unidentified, factor(s) in the altered calcium metabolism which accompanies lactation. In the present study, we investigated the possibility that PTH-related protein (PTHrP), which is produced in lactating mammary glands, is a putative calciotropic factor acting systemically during lactation. To test this hypothesis, we examined changes in urinary phosphate and cAMP excretion in relation to suckling since phosphaturia (P-uria) and increased urinary cAMP excretion are sensitive parameters of PTHrP action on the kidney. When lactating rats (separated from their pups overnight) were allowed to suckle pups for 1 h, they showed a marked P-uria which lasted 3-4 h. In most instances, a transient increase in cAMP excretion preceded the P-uria. These effects were not abolished by thyroparathyroidectomy; hence they are not attributable to a transient increase in PTH secretion. Administration of PRL or oxytocin did not induce significant P-uria. When lactating rats were pretreated with anti-PTHrP anti-serum, the suckling-associated P-uria was prolonged and augmented. This prolongation of P-uria was similar to the effects observed when exogenous PTHrP (1-34)amide was administered in the presence of the antiserum. These data support the hypothesis that some of the PTHrP produced in lactating mammary glands may be released systemically during suckling and act in an endocrine manner on target organs such as the kidney.
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PMID:Suckling-mediated increases in urinary phosphate and 3',5'-cyclic adenosine monophosphate excretion in lactating rats: possible systemic effects of parathyroid hormone-related protein. 165 80

A high level of Ca2+ or Mg2+ nucleotide phosphohydrolase activity is present on the outside surface of intact myometrial cells and is also observed in the isolated plasma membranes. About half of this activity is labile while the remainder is stable. The characteristics of the activities suggest the presence of at least two different ecto-enzymes. The stable component (Km for Ca2+ about 0.1 mM) accepts XTP or XDP as substrate, is not inhibited by p-chloromercuriphenylsulfonate or inorganic phosphate, but is inhibited by 20 mM NaN3. The labile component (Km for Ca2+ nearly 1 mM) cleaves XTP but not XDP, and is inhibited by p-chloromercuriphenyl-sulfonate and inorganic phosphate, but not by NaN3. The activity of the labile component can be restored by removing the cells from the incubation medium and resuspending them in fresh medium. This suggests that the 'lability' is due to product inhibition, probably by inorganic orthophosphate. While the Ca2+ pump of myometrial plasma membranes was inhibited by 0.1 microM oxytocin, these ecto-enzymes were unaffected by oxytocin concentrations up to 10 microM. Because of its high activity and rapid inactivation by product inhibition, the labile enzyme may be involved in the regulation of purinergic receptors.
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PMID:Ca2+ or Mg2+ nucleotide phosphohydrolases in myometrium: two ecto-enzymes. 166 Nov 50


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