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)

Placental steroid sulfatase deficiency is an unusual cause of low estriol production during pregnancy. Its importance lies in the differentiation of this disorder from the more ominous fetal defects that result in low estriol levels. Serum free estriol levels were found to be low or absent in a 25-year-old gravida 3, para 2 woman, while placental lactogen and chorionic gonadotropin levels were normal. An abdominal x-ray revealed no apparent congenital abnormalities and an oxytocin challenge test was negative. The dehydroepiandrosterone sulfate (DHEA-S) level in the patient's amniotic fluid was 6.8 to 18.4 times greater than those found in control amniotic fluids. The patient's amniotic fluid cortisol level was normal. Twenty-four hours following a normal, spontaneous labor and delivery at 39 weeks, the male infant underwent a synthetic ACTH1-24 stimulation test, with serum cortisols rising from 3.7 to 46 mug/dl at 1 hour. The placenta was morphologically normal on gross, light, and electron microscopic examinations. Steroid 3-alcohol sulfatase and arylsulfatase activities in the patient's placenta were virtually absent. These data indicate that this benign cause of low serum estriol levels may be diagnosed prenatally by elevated amniotic fluid DHEA-S levels.
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PMID:Prenatal diagnosis of placental steroid sulfatase deficiency. 13

In the external layer of the median eminence of the fox, the somatostatin-containing fibers and neurophysin-containing fibers of the hypothalamo-infundibular tract are located in distinct areas. In the neural lobe, somatostatin-positive areas are simultaneously neurophysin-positive. Outside the SON and PVN, some somatostatin-positive and neurophysin-negative perikarya are scattered close to the third ventricle. These facts suggest the existence of two somatostatin systems: a hypothalamo-infundibular (neurophysin-negative) one and a hypothalamo-neurohypophyseal (neurophysin-positive) one.
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PMID:[Somatostatin-containing fibers and neurophysin-containing fibers in the median eminence of the fox, as seen with a double staining cytoimmunoenzyme technique]. 14 93

The Eisenmenger syndrome carries a high mortality rate in a women during delivery and the immediate postpartum period. It has been suggested that marked changes in shunt flow and pulmonary hemodynamics may be responsible. These functions were studied under various physiologic and pharmacologic conditions during labor and delivery in a patient with the Eisenmenger syndrome. Uterine contractions were associated with a decrease in the ratio of pulmonary to systemic blood flow (Qp/Qs) from 1.58 to 1.05. The Qp/Qs ratio also decreased (to 0.83) when forceps were applied during uterine contractions. Epidural anesthesia, oxytocin and the supine position did not adversely affect pulmonary hemodynamics or shunt flow. On the basis of these results, if pregnancy cannot be terminated in a patient with the Eisenmenger syndrome, it is recommended that the patient be given high concentration of oxygen and epidural anesthesia and that serial arterial blood gas determinations be performed to detect changes in shunt flow.
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PMID:Shunt flow and pulmonary hemodynamics during labor and delivery in the Eisenmenger syndrome. 15 Jul 87

The enhancement of the response of an isolated strip of lactating mouse mammary gland to oxytocin, resulting from dilution of the Tyrode solution in which oxytocin is administered, is due to the effects of hypotonicity per se and not to changes in concentration of any of the ions in the bathing solution. Inhibition of membrane ATPase also causes an enhancement, which is probably due to activation of a secondary facilitating mechanism, rather than to enhancement of the entire train of oxytocin-induced reactions. A variety of conditions which alter the response to oxytocin have the same effect on the response to acetylcholine. Hypotonicity can therefore increase the sensitivity of this bioassay for oxytocin, but not its selectivity.
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PMID:Action of oxytocin on mammary gland: influence of hypotonicity. 15 60

Prostaglandins are highly potent derivatives of unsaturated fatty acids with multiple biological activities. They are synthesized and metabolized in almost all tissues studied so far. The E- und F-type prostaglandins may be regarded as local modulators of hormonal effects on cell function and--in some cases (kidney, uterus-corpus luteum)--as regional or tissue hormones. Thus they seem to be involved in the regulation of neurotransmission, kidney function, triglyceride metabolism in adipose tissue and progesterone biosynthesis. Apart from their influence on renal blood flow prostaglandins of the A-type possibly have an additional function as circulatory hormones regulating blood pressure. Second messenger-systems (cAMP, Ca++-cGMP) which mediate the effects of most non-steroidal hormones are also involved in the action of prostaglandins, at least of the E-and F-types. Disturbances in prostaglandin metabolism (increased or decreased biosynthesis) are discussed to play a role in the pathogenesis of inflammation, pain, fever, hypertension, bronchial asthma and gastric or duodenal ulcer formation. Drugs with antiinflammatory, analgesic and antipyretic activity have been shown to be potent inhibitors of prostaglandin formation. The correlation of a local prostaglandin deficit or the therapeutic use of single effects of prostaglandins by administration of exogenous compounds (natural prostaglandins or modified derivatives) has so long been less satisfactory because of their large number of biological actions which lead to undesired side effects. Extensive experience have been obtained in the successful induction of therapeutic abortion. This effect is based on the stimulatory action of E- and F-type prostaglandins on the smooth muscles of the pregnant uterus which is resistent to the influence of other stimuli, e. g. oxytocin. Here the incidence of side effects could be reduced by local administration of low doses of prostaglandins into the uterine cavity. A general improvement of the therapeutic usefulness of prostaglandins will however only be achieved, if modified derivatives with more specific actions on the desired "target" tissues are available.
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PMID:[Biology of prostaglandins with reference to therapeutic aspects]. 16

This investigation was undertaken to evaluate the functional contribution of the peptide backbone of oxytocin in its interaction with receptor. Corey-Pauling-Koltun models of (Gly-7) deaminooxytocin, deaminotocinamide, and their respective retro-D-analogs built in any specific conformation (e.g., the Walter-Urry model for oxytocin) have a quai-equivalent topochemical arrangement of amino-acid side chains; however, the CO and NH elements of the peptide backbone of the retro-D-analog are reversed. The retro-D-analogs of deaminotocinamide and (Gly-7) deaminooxytocin (prepared using D-alle for L-Ile) and their respective N-formyl derivatives were assayed for uterotonic activity relative to related L-peptides. All retro-D-analogs (tested at concentrations ranging from 10-10 to 10-5 M) were devoid of angonistic (or antagonistic) activity in the isolated rat uterus, except for the retro-D-(D-alle-3, Gly-7) deaminooxytocinamine, which retains a terminal NH-2 group on the tail; the latter is a partial agonist with very low affinity. The results obtained with retro-D-analogs indicate that one or more of the elements of the peptide backbone of the tocinamide ring are essential for "occupation" and "activation" of uterine receptors. Oxytocin action may be the resultant of multiple hydrogen-bonding interactions between CO, NH, NH-2, and OH groups of the hormone with complementary groups on receptor, made possible by appropriate hydrophobic bonding.
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PMID:Contribution of the peptide backbone to the action of oxytocin analogs. 16 58

[3-H]Oxytocin was incubated in vitro with pieces of oviduct and mammary gland and the tissue were subjected to autoradiography. Radioactivity was localized only in smooth muscle cells of the oviduct and in regions of mammary tissue where myoepithelial cells are found. In contrast, radioactivity was not concentrated in any region of skeletal muscle, a nontarget tissue for oxytocin. The localization of radioactivity in oviduct and mammary cells was absent when the tissues were incubated with [3-H]oxytocin and an excess of unlabeled oxytocin. These findings provide evidence for the presence of specific and high affinity receptors for oxytocin in its target tissues.
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PMID:Autoradiographic localization of radioactivity from [3-H]oxytocin in the rat mammary gland and oviduct. 16 62

CAMP levels of isolated rat uteri (2nmol/g wwt) were increased by Fenoterol (10(-4)--1 mug/ml) in a dose dependent manner reaching concentrations of more than 10nmol/g withing 2--5 min. AT 2 TIMES 10(-3) MUG/ML Fenoterol inhibited spontaneous contractions of the rat uterus in vitro. A 10,000 fold higher dosis of Fenoterol was needed to elicit a similar degree of inhibition, when contractions were induced by 0.6 mU/ml Oxytocin. However cAMP levels were elevated by Fenoterol in presence of Oxytocin, uterine contractions were not inhibited, i.e. the elevation of cAMP after administration of Fenoterol is correlated with a relaxant effect only in uteri contracting spontaneously.
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PMID:[Influence of fenoterol of cAMP levels and motility on the rat uterus in vitro (author's transl)]. 16 93

3H-corticoids were localized by autoradiography in small neurons in the area of the magnocellular paraventricular nucleus of mallard ducks. Correlative data show that: (1) the label is principally unmetabolized steroid, (2) the hypothalamus competitively binds corticosterone, (3) the paraventricular nucleus contains immunoreactive neurophysin, is richly innervated by boutons of monoaminergic nerves and is involved in the adaptive response to osmotic stress.
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PMID:Corticoid uptake by the paraventricular nucleus in the hypothalamus of the duck, Anas platyrhynchos. 16 95

The binding of 3H-labelled neurohypophyseal nonapeptide hormone, oxytocin, to isolated rat fat cells has been measured under conditions where this compound elicits the known activation of glucose oxidation by these cells, called "insulin-like" action. Uptake by the cells of the [3H]peptide as a function of various concentrations of the hormone in the medium indicated the presence of two classes of binding sites with different apparent affinities and capacities. The sites of the first type exhibit a rather high affinity, but low capacity, for oxytocin (5 nM; 3 X 10(4) sited per cell) and appear to be saturable under a reversible process. Evaluation of dose-response relationships suggest that they may be directly related to the measured biological response (i.e. activation of the glucose to 14CO2 conversion). Competition experiments show that [3H]oxytocin binding to the cells remains constant within a large range of insulin concentrations. The apparent capacity of different hormone analogs to compete with oxytocin for binding to this class of receptors has been evaluated and compared with the measured insulin-like activity of these different compounds. The sites of the second category have significantly lower affinity, but higher capacity for oxytocin, and were found to be not saturable under the experimental conditions. [3H]Oxytocin uptake by ghosts prepared from the isolated fat cells showed striking similarities to the binding process described for whole cells, although the affinity and total capacity of the former were found to be slightly lower. The basal and adrenalin-stimulated adenylate cyclase of these fractions appeared to be unaffected by various concentrations of oxytocin. It is concluded that there may exist on the rat fat cell membranes a discrete number of oxytocin receptors possessing high specificity for oxytocin and exhibiting affinities and kinetic behaviour similar to those of other characterized oxytocin receptors. They are believed to be independent of the other hormonal receptors of the rat fact cells.
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PMID:Characterization of oxytocin receptors on isolated rat fat cells. 17 Jan 3


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