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)

1. A technique is described for obtaining a myometrial preparation devoid of endometrium, from the uterus of the rat in oestrus. 2. Acetylcholine and prostaglandin F2alpha (PGF2alpha) produced concentration-effect curves with the same maximal tensions and slope on the whole uterus and myometrial preparations. Concentration-effect curves to bradykinin and oxytocin on the myometrial preparation were altered, resulting in a shift to the right and a decreased maximum response compared with those produced by the whole uterus. 3. Indomethacin produced greater antagonism of the responses of the whole uterus to bradykinin and oxytocin than to acetylcholine and PGF2alpha, whereas responses of the myometrium to all four agonists were similarly depressed. 4. Responses of the myometrial preparation to a range of concentrations of bradykinin and oxytocin were significantly enhanced by prior sensitization of the myometrium to PGF2alpha. This significant enhancing effect of PGF2alpha was only seen with the threshold dose of acetylcholine. 5. It appears that the mechanism of action of bradykinin and oxytocin on the rat uterus involves both a direct action and an indirect action. The indirect action possibly involves release of prostaglandin(s) from the endometrium.
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PMID:The action of bradykinin and oxytocin on the isolated whole uterus and myometrium of the rat in oestrus. 56 12

An attempt was made to postpone term in 59 pregnant rats by s.c. injections of indomethacin or cyproheptadine, or a combination of both. The cyproheptadine group gave birth to their litters on days 20-22, yet indomethacin postponed labour to the 23rd day, both when given alone or in combination with cyproheptadine. As the fourth saline group went into labour on the 20--23rd day the indomethacin postponement cannot be considered significant. Indomethacin being a prostaglandin antagonist and cyproheptadine a serotinin antagonist, it may be concluded that neither prostaglandin nor serotonin are decisive for the intricate process which triggers parturition. Other factors, such as decrease of progesterone, increase of oestrogen and perhaps foetal oxytocin, as well as placental ACTH, seem to concur in inducing labour, their effect being fortified by serotonin and prostaglandins during parturition.
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PMID:Effect of indomethacin and cyproheptadine on onset of labour in rats. 86 38

Treatment of pregnant rats with 1 mg indomethacin/kg twice daily i.m. beginning on Day 20 delayed the onset of parturition by about 21 hr and prolonged the duration of spontaneous parturition by 4 hr. Plasma progesterone and oestradiol levels were determined in daily samples of peripheral blood, and uterine contractions were recorded before and during parturition by means of small, chronically implanted intrauterine balloons which were connected to pressure transducers via fluid-filled catheters. Indomethacin treatment did not inhibit or suppress spontaneous or oxytocin-induced contractions, which were of the same intensity in indomethacin-treated as in control rats. Parturition was induced with oxytocin in the same proportion of treated and control rats, but its induction was not successful in treated rats until 1 day later than in control rats, but its induction was not successful in treated rats until 1 day later than in controls. The onset of parturition was always related to the plasma progesterone level, which declined at a slower rate in indomethacin-treated than in control rats, reaching baseline values approximately 1 day later in the treated animals. The appearance of 20alpha-hydroxysteroid dehydrogenase in the CL of pregnant rats normally occurs on Day 21 of gestation, but activity was not observed until about 1 (0-3) day later in the indomethacin-treated rats, indicating that luteolysis was retarded. Prostaglandin F-2alpha infusions given on Day 21 reversed the effects of indomethacin treatment on plasma progesterone, luteal 20alpha-hydroxysteroid dehydrogenase activity and the timing and duration of parturition, and reduced the high perinatal mortality associated with indomethacin treatment, suggesting that the effects of indomethacin were related to its inhibitory action on prostaglandin synthetase activity. It is concluded that, in rats, indomethacin exerts its effects on parturition through inhibition of luteal regression which was significantly retarded but not prevented, and that indomethacin does not have a direct effect on myometrial contractility.
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PMID:The effect of indomethacin on uterine contractility and luteal regression in pregnant rats at term. 103 79

In a previous report we demonstrated the presence of a vasotocin (AVT)-like peptide in chromaffin cells of the amphibian adrenal gland and showed that synthetic AVT is a potent stimulator of corticosterone and aldosterone secretion by frog adrenocortical cells. In the present study we evaluated the relative potency of various AVT analogs and investigated the mechanism of action of AVT on frog interrenal (adrenal) tissue. Several AVT agonists, including hydrin 2, oxytocin (OXT), arginine vasopressin (AVP), Lys-conopressin G, and mesotocin (MT), were able to mimic the stimulatory effect of AVT on steroid secretion, but AVT was by far the most potent stimulator of steroidogenesis. In the series of analogs studied, the order of potency was: AVT greater than hydrin 2 greater than OXT greater than AVP greater than Lys-conopressin G greater than MT greater than [deamino-Cys1,D-Arg8]AVP greater than [d(CH2)5,Tyr(OMe)2] AVP. The effect of AVT (5 x 10(-10) M) was totally blocked by both the antidiuretic V2 antagonist [d(CH2)5,D-Phe2,Ile4,Ala9-NH2]AVP (10(-6) M) and the oxytocinergic antagonist [d(CH2)5,Tyr(OMe)2,Orn8]AVT (10(-6) M); the V2 antagonist was approximately twice as potent as the OXT antagonist. In contrast, the V1 antagonist 1-(1-mercapto-4-phenylcyclohexaneacetic acid)-AVP (10(-6) M) did not affect the response of the interrenal tissue to AVT. Indomethacin (5 microM), a cyclooxygenase inhibitor, induced a dramatic decrease in the spontaneous secretion of corticosteroids, but did not impair the stimulatory effect of AVT (5 x 10(-9) M) on corticosterone and aldosterone secretion. In addition, AVT did not stimulate the production of prostaglandin E2, suggesting that prostaglandins are not involved in the mechanism of action of AVT. Concurrently, AVT did not modify cAMP production by frog adrenal slices. In contrast, AVT induced both an increase in inositolphosphate production and a reduction of membrane phospholipid content. We conclude that in the frog adrenal gland, the stimulatory effect of AVT on steroid secretion is mediated through activation of receptors related to the mammalian V2 and/or OXT receptors, which are positively coupled to phosphoinositide-specific phospholipase C.
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PMID:Pharmacological characterization of vasotocin stimulation of phosphoinositide turnover in frog adrenal gland. 130 45

Two experiments were performed to determine whether arginine vasotocin (AVT) stimulates synthesis of prostaglandins (PGs) in reptilian oviducts. Homogenized oviducal tissue from female Sceloporus jarrovi in early and late pregnancy were cultured with radiolabeled (14C) prostaglandin precursor, arachidonic acid (AA). In late pregnancy, oviducts exposed to AVT exhibited a greater conversion of AA to PGF2 alpha than did controls, whereas in early pregnancy there was no difference. The conversion of AA to other prostaglandins (PGA2, PGD2, PGE2, PGI2) was not influenced by AVT. The second experiment examined whether endogenous in vitro synthesis of PGF and PGE2 from intact, pregnant oviducts was stimulated by AVT (50 ng/ml; 100 ng/ml). Both doses of AVT induced a similar, significant rise in PGF concentrations within 30 min whereas no significant increase was noted in PGE2 concentrations until 90 min after treatment. Indomethacin pretreatment blocked synthesis of both PGF and PGE2 for 30 min following AVT treatment. These data indicate that AVT induces a highly specific rise in the synthesis of PGF from the oviduct of female S. jarrovi in late pregnancy. Furthermore, the prostaglandin-stimulating effect of AVT in reptiles appears homologous with the effect of oxytocin in mammals and AVT in birds. We hypothesize that this interaction is an evolutionarily conserved relationship found in all amniote vertebrates.
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PMID:Arginine vasotocin-induced prostaglandin synthesis in vitro by the reproductive tract of the viviparous lizard Sceloporus jarrovi. 230 42

The ligamentum infundibulo-cornuale (LIC) in the pig runs along the anterolateral side of the tubal isthmus, connecting the uterotubal junction and the edge of the infundibulum and has a comparatively well-developed muscular component running under the mesothelium. The well-vascularized smooth muscle cells held close cell-to-cell contacts and received innervation by adrenergic and cholinergic-like nerve terminals. Isolated LIC preparations, collected during oestrus showed a rhythmic spontaneous motility in vitro, the frequency and the relative amplitude of the contractions being highest during the preovulatory period. In vitro, noradrenaline and adrenaline elicited contractile (alpha) and relaxatory (beta) responses, while isoprenaline induced only beta-responses, as demonstrated by pretreatment with selective blockers. Oxytocin, PGF2 alpha and PGE2 always increased the muscular activity of the LIC. Indomethacin inhibited, in a concentration-dependent and reversible manner, the spontaneous motility of the porcine LIC, which could be fully restored by PGF2 alpha, indicating an endogenous local synthesis of prostaglandins in the tissue. The present results suggest that, in the pig, the LIC consists of a well-arranged, richly innervated bulk of smooth muscle which shows rhythmic spontaneous activity at the time of ovulation that could assist ova pick-up.
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PMID:The ligamentum infundibulo-cornuale in the pig: morphological and physiological studies of the smooth muscle component. 236 2

Indomethacin and substance BW-755C in experiments on isolated myometrium striae of pregnant white rats exert an inhibiting effect on the contractile uterus function due to inhibition of cyclooxygenase or lipoxygenase ways of the arachidonic acid transformation. Prostaglandin F2 alpha is sensitive to functioning of the cyclooxygenase and lipoxygenase ways of the arachidonic acid transformation, while oxytocin--only lipoxygenase one. Conclusions rest on results from multiparametric analysis of the contractile uterus function suggested by authors and confirmed by the pattern recognition method--the Karunen-Loev orthogonal decomposition.
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PMID:[Comparative evaluation of the action of prostanoid inhibitors on uterine contractile function]. 250 61

1. The actions of angiotensin II, bradykinin, oxytocin, arginine vasopressin, relaxin, serotonin and the prostaglandins E2 and F2 alpha were examined on preparations of costo-uterine muscle from stilboestrol-treated rats. 2. All the agonists, except relaxin, when used in concentrations which contract the rat uterus, also produced contractions of costo-uterine muscles. Concentration-response curves were steep and maximal responses to the agonists were comparable. The negative log molar EC50 values were: serotonin, 6.5; angiotensin II, 8.8; bradykinin, 8.4; PGE2, 8.3; PGF2 alpha, 7.1. The EC50 values (units/L) for oxytocin and vasopressin were 4.4 and 2.7 respectively. 3. Indomethacin (2.8 or 5 mumol/L) did not decrease the contractile effects of the peptides or serotonin. The effects of serotonin were reduced, but not reversed, by methysergide (0.94 mumol/L). 4. Porcine relaxin inhibited field stimulation-induced contractions of costo-uterine muscle and uterine horns from immature rats pretreated with oestradiol cypionate and from stilboestrol-treated mature rats. It was much less potent, and its effects were less clearly concentration-related, on costo-uterine muscle. 5. The inhibitory effects of relaxin on the uterus were unaffected by propranolol (1 mumol/L), confirming that on this tissue relaxin acts independently of the release of catecholamines. Progesterone (30 mumol/L) was also without effect on the action of relaxin on the uterus. 6. These results taken together indicate that the costo-uterine muscle of the rat: (i) contracts in response to serotonin and the peptides angiotensin II, arginine vasopressin, bradykinin and oxytocin independently of the release of the contractile prostaglandins F2 alpha and E2; and (ii) in contrast to the uterus, may lack a significant population of receptors for relaxin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Actions of some autacoids and peptides, including relaxin, on costo-uterine muscle from rats. 257 64

Oxytocin (OXY) is a nonapeptide of hypothalamic origin which has defined roles in the female reproductive functions of lactation and labor. However, OXY may have other physiological functions because of its presence in the male and its release in response to stress. Available evidence suggests prostaglandins may stimulate the release of OXY. These experiments sought to determine if the stressors, endotoxin and hemorrhage, would release OXY in the chronically catheterized, freely behaving male rat and what effect the antipyretic and prostaglandin synthesis inhibiting drug, indomethacin, would have on these responses. Endotoxin caused a marked release of OXY from mean baseline levels of 5 pg/ml to mean peak levels of 168 pg/ml. Indomethacin greatly attenuated this increase. In contrast, OXY release in response to hemorrhage of either 22 or 44% of the blood volume of the rat was enhanced by indomethacin. Indomethacin increased the hemorrhage-induced OXY levels about 2-fold over a 2-hour posthemorrhage period. Indomethacin alone had no effect on OXY levels. These data verify that stress is a potent stimulus for OXY release and strengthen the hypothesis that prostaglandins mediate OXY release. The paradoxical effects of indomethacin on OXY release suggest that the prostaglandins may have different effects on OXY release depending upon the evoking stimulus.
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PMID:Indomethacin, an antipyretic drug, prevents the endotoxin-induced and potentiates the hemorrhage-induced oxytocin release into the plasma of the male rat. 351 21

Experiments were conducted to determine the effects of infusing indomethacin, a prostaglandin synthetase inhibitor, into the uterine lumen on the development and function of the bovine corpus luteum in the presence and absence of concurrently administered oxytocin. Each treatment was given twice daily on d 4, 5 and 6 of the estrous cycle. Treatments (six heifers/group) and resulting estrous cycle lengths were as follows: (1) untreated controls, 20.6 +/- .4 d; (2) .2 M phosphate buffer vehicle infused into the uterine lumen, 21.0 +/- .6 d; (3) 40 mg indomethacin infused into the body of the uterus, 16.5 +/- 1.0 d; (4) 150 USP units oxytocin injected sc, 10.0 +/- 1.2 d and (5) a combination of oxytocin and indomethacin as in treatments 3 and 4, 14.1 +/- 1.3 d. Plasma concentrations of progesterone were lower (P less than .05) in each treatment group from d 7 onward, when compared with untreated and vehicle-treated controls. Indomethacin alone effectively inhibited the development and function of the corpus luteum, and was without effect on oxytocin-induced inhibition of luteal function. In summary, it appears that a prostaglandin of either uterine or ovarian origin, or both, is required for the normal development and function of the bovine corpus luteum.
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PMID:Inhibition of bovine luteal function by indomethacin. 403 10


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