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)

Porcine relaxin (250 guinea-pig units/mg) infused intravenously into anaesthetized rats at 20 micrograms/h reversibly abolished spontaneous intra-uterine pressure cycles yet left the myometrium responsive to oxytocin in doses of 4--8 mu. The inhibition was found to be primarily of the frequency, rather than of the amplitude, of pressure cycles. Relaxin (5 or 10 micrograms) was capable of completely suppressing uterine activity driven by prostaglandin F2 alpha infusion in oestrogen-treated ovariectomized rats. Whereas the beta-adrenergic blocker, propranolol, had no effect on relaxin-induced inhibition, phentolamine, an alpha-blocker, significantly delayed the relaxin effect. It is unlikely, however, that relaxin operates through an alpha-inhibitory receptor. The results show that relaxin acts primarily as a frequency modulator and is capable of antagonizing an exogenous myometrial stimulant.
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PMID:Relaxin inhibits spontaneous and prostaglandin-driven myometrial activity in anaesthetized rats. 52 35

Paired segments of rat uterus were treated in vitro with relaxin (W1164-3, 150 GPU/mg) until the amplitude of contraction was reduced to at least 50% of the pre-treatment amplitude. Test segments then received 100 ng of either PGE1, PGE2, PGF2alpha or 250 uU of oxytocin. Control segments remained untreated. There was a significant increase in contraction amplitude in response to the spasmogens (P less than 0.05) but no increase was seen in controls.
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PMID:In vitro response of relaxin-treated rat uterus to prostaglandins and oxytocin. 59 78

When post-partum ovariectomized rats were linked to 21-day-pregnant rats by a cross-circulation system their myometrial activity was almost completely inhibited. No reduction in activity was induced by cross-circulation with other post-partum rats, or with rats in which myometrial activity had been suppressed with oestrogen. Changes in uterine activity could not be correlated with alterations in arterial blood pressure occurring during the experiments. Uteri rendered inactive by cross-circulation were found to be responsive to oxytocin. It is concluded that a humoral myometrial inhibitor is present in late pregnancy in rat blood and the possibility that it is relaxin is discussed.
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PMID:Evidence that a humoral factor possessing relaxin-like activity is responsible for uterine quiescence in the late pregnant rat. 62 4

Our previous studies implicated the involvement of protein kinase-A in the inhibitory effects of isoproterenol and relaxin on oxytocin-stimulated phosphoinositide turnover in rat myometrium. To understand the possible mechanisms involved, the properties and regulation of phospholipase-C (PLC) in purified myometrial plasma membranes from estrogen-primed rats were studied. The PLC activity measured with exogenous [3H]phosphatidylinositol 4,5-bisphosphate as substrate was Ca2+ dependent. The nonhydrolyzable GTP analog guanosine 5'-(3-O-thio)triphosphate stimulated PLC activity with a ED50 of 1.6 microM and shifted the calcium dependence curve to the left. Guanosine 5'-(3-O-thio)triphosphate-stimulated phosphatidylinositol 4,5-bisphosphate hydrolysis was inhibited by activation of endogenous and exogenous cAMP-dependent protein kinase (PKA). The effects of endogenous and exogenous PKA were significantly reversed by IP20, a potent synthetic peptide inhibitor of PKA. In the presence of [gamma-32Pi]ATP and exogenous PKA, 32Pi was incorporated in an IP20-sensitive manner into major bands at approximately 17,000, 20,000-24,000, 33,000, 38,000, 40,000-44,000, and other higher mol wt. These data indicate that one or more GTP-binding proteins mediate activation of membrane-bound PLC in rat myometrium. Phosphorylation of one or more membrane-associated proteins by PKA may regulate myometrial PLC activity and play a role in the inhibitory effects of isoproterenol and relaxin.
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PMID:Protein kinase-A inhibits phospholipase-C activity and alters protein phosphorylation in rat myometrial plasma membranes. 132 60

The influence of treatment with oestradiol on the effects of the uterine relaxants, relaxin, salbutamol (an agonist at beta 2-adrenoceptors) and cromakalim (a potassium channel opener) and their interactions with the uterine stimulant oxytocin were investigated in vivo in the ovariectomized rat. Oestradiol benzoate (0.4 micrograms/kg per day) significantly increased sensitivity to cromakalim as an inhibitor of spontaneous uterine contractions compared with vehicle-treated rats by approximately threefold. The same dose of oestradiol benzoate had no effect on uterine sensitivity to salbutamol. Previous studies have shown that this dose of oestradiol benzoate produces a twofold increase in uterine sensitivity to relaxin as an inhibitor of spontaneous contractions. Oestradiol influenced the ability of relaxin to inhibit oxytocin-stimulated uterine contractions. In corn oil-treated rats, uterine responses to relaxin were markedly reduced during oxytocin infusion compared with responses to relaxin before oxytocin; the maximum obtainable response to relaxin was less than 50% inhibition. In oestradiol-treated rats, uterine sensitivity to relaxin during oxytocin infusion was similar to that observed against spontaneous contractions. Cromakalim was able to inhibit uterine contractions during oxytocin infusion in both corn oil- and oestradiol-treated rats, uterine sensitivity to cromakalim being similar in the absence and presence of oxytocin for both hormone treatment groups. Salbutamol was also able to inhibit uterine contractions during oxytocin infusion in both corn oil- and oestradiol-treated rats. Oestradiol treatment increased the potency of salbutamol as an inhibitor of oxytocin-stimulated uterine contractions compared with corn oil treatment by 3.5-fold. The interaction of oestradiol and relaxin during late pregnancy may be important for attenuation of the myometrial response to stimulants.
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PMID:Interaction between myometrial relaxants and oxytocin: a comparison between relaxin, cromakalim and salbutamol. 143 80

Oxytocin was measured in incubates and perifusates of neurosecretosomes prepared from sow neural lobes (n = 50) and in incubates of isolated neural lobes (n = 5). In none of these preparations was oxytocin output affected by exposure to purified porcine relaxin (at concentrations up to 10(-7) mol l-1). Moreover, in lactating sows (n = 9), 6-10 days post partum, the administration of porcine relaxin (1.5 or 3.0 mg) intravenously, immediately before a suckling episode, did not affect the plasma oxytocin profile compared with saline treatments (within sow) nor did it alter suckling behaviour or the weight gain of the litter. In all sows, a spike (25-75 pg ml-1) of oxytocin was measured during milk ejection coincident with suckling. These results suggest that porcine relaxin does not affect oxytocin release in suckling sows in contrast to reported findings in rats. The data also support the view that porcine relaxin could be used at farrowing without adverse effects on suckling.
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PMID:Lack of effect of relaxin on oxytocin output from the porcine neural lobe in vitro or in lactating sows in vivo. 143 57

After parturition, eight sows were zero weaned by removing all piglets 6 h after birth; a further 18 sows suckled at least ten piglets each. Blood samples were collected on Day 4 after zero weaning or on Days 4, 14 and 21 of lactation and the sampling frequency increased during suckling bouts. Ovaries were recovered from sows on these days and corpora lutea were either extracted for estimation of relaxin and progesterone concentration, fixed for immunohistochemical analysis or incubated in vitro in the presence or absence of luteinizing hormone (LH) or oxytocin. Luteal weight and progesterone were higher in the zero-weaned sows than in lactating sows (P less than 0.05 and less than 0.001, respectively); relaxin content was below detection by Day 14. This was supported by immunohistochemical staining for relaxin, which showed limited immunostaining in zero-weaned and Day 4 sows, but none in the tissue recovered on Days 14 and 21, which showed typical signs of regression. Secretion of progesterone and relaxin by luteal tissue in vitro was highest in zero-weaned sows (P less than 0.05), decreased as lactation progressed and neither LH nor oxytocin had any significant effect. Concentrations of plasma relaxin were all less than 0.2 ng/ml in three of the four zero-weaned and Day-4-suckled sows assayed; there was no detectable increase during suckling bouts. It was concluded that during lactation the old corpus luteum of pregnancy is not able to release relaxin in response to suckling in vivo or to oxytocin treatment in vitro.
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PMID:Lack of stimulation of relaxin secretion in lactating sows by suckling in vivo or by oxytocin in vitro. 155 73

Equine relaxin has been previously determined in a small number of pregnant Thoroughbred mares. To better define the normal pregnancy pattern of relaxin, the current study reports on a much larger number of mares. It also was designed to determine if all equids have the same gestational pattern of relaxin secretion. Plasma samples were collected weekly in 24 Standardbred mares, every 7-10 days in 10 pony mares, and daily in late pregnancy from 16 burros. Standardbreds had higher concentrations of relaxin than that reported for Thoroughbreds during most of gestation and did not exhibit the midpregnancy nadir in relaxin concentrations observed in Thoroughbreds. Relaxin concentrations in Standardbreds showed a small but steady decline from Day 150 until delivery. Pony mares had lower relaxin concentrations throughout pregnancy than other mares and had continuously increasing concentrations during gestation. Burros had relaxin concentrations intermediate to ponies and other mares in late gestation. Burros induced to foal with oxytocin showed a sharp increase in relaxin concentrations. No effect of the sex of the offspring was observed in relaxin profiles in Standardbred mares. Each of three Standardbreds with abnormal termination of pregnancy exhibited abnormally low relaxin concentrations at some point in the gestation prior to termination of the pregnancy. Thus, relaxin may be an indicator of placental functioning and used to assess at-risk pregnancies in mares.
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PMID:Breed differences in circulating equine relaxin. 157 61

The discovery of the various peptide factors in the gonads followed different paths. A number of factors were specifically searched for because of physiological experiments that predicted that an activity from the gonads was necessary to explain phenomena. Such was the case for gonadal steroids and for such peptide factors as inhibin, MIS, OMI, FRP, seminal plasma inhibin, relaxin, PA factor and other proteases, and ABP. In the process other factors such as activin and follistatin were serendipitously discovered. A second group of factors was discovered because in vitro experiments of various combinations of gonadal cell types failed to replicate in vivo findings, suggesting missing signals. Such substances are the panoply of growth factors aiding in differentiation and growth promotion and inhibition: LS and LI, P-Mod-S, clusterin, and various components of the ECM. Finally, and most recently, another set of peptides has been identified because immunological or molecular probes have been used to search gonadal tissue for factors originally discovered elsewhere; these include POMC, GnRH-like peptide, oxytocin, AVP, angiotensin, ANF, CRF, neural peptides, and c-mos. Our understanding of the relationship of most of these peptides to the local signals necessary for gonadal function is still very elementary. Clearly some like relaxin and inhibin function as important hormones, and ABP, for example, probably functions importantly in transporting testosterone down the tubule. Most local paracrine or autocrine peptide signals appear to act in relationship to gonadotropin levels probably in local differentiation in the process of gamete maturation, but this is only conjecture at this point. No experimental verification that any of these factors is involved in follicle selection for recruitment or for atresia is yet available. For many of the factors local receptors have not yet been identified. The richness of the variety of peptides in the gonads suggests that microanalysis of cell-cell signaling would be rewarding, but at the time of this writing such investigations are not yet possible.
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PMID:Nonsteroidal signals originating in the gonads. 162 34

In urethane-anaesthetized ovariectomized rats, injection of porcine relaxin (7.5 and 15 micrograms/kg, i.v.) caused a sustained increase in circulating plasma oxytocin and vasopressin concentrations; 10 micrograms relaxin/rat i.v. produced a smaller but significant increase in plasma oxytocin concentration in conscious ovariectomized rats. A significant increase in oxytocin concentration and inhibition of the spontaneous milk-ejection reflex was also seen in anaesthetized (ovary intact) lactating rats following injection of relaxin (7.5 micrograms/kg, i.v.). To investigate whether relaxin acts by increasing the electrical activity of oxytocin neurones or by facilitating stimulus-secretion coupling in the pituitary, the electrical activity of neurones in the supraoptic nucleus was recorded in urethane-anaesthetized lactating rats and in ovariectomized rats. Porcine relaxin (10 micrograms/rat, i.v.) increased the firing rate of both oxytocin and vasopressin neurones in the supraoptic nucleus in lactating rats. The response to relaxin was unaffected by subsequent injection of naloxone (1 mg/kg, i.v.). Oxytocin neurones were also activated by injection of relaxin (10 micrograms/rat) into ovariectomized rats. Combining the electrophysiological data, the neuronal activation following relaxin was significantly correlated with the level of spontaneous activity prior to relaxin injection. The results show that relaxin acts centrally to increase circulating plasma oxytocin and vasopressin concentrations by an opioid-independent mechanism.
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PMID:Relaxin increases the firing rate of supraoptic neurones and increases oxytocin secretion in the rat. 173 54


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