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)

Vasopressin, vasopressin analogs, forskolin and 8-bromo-cyclic AMP (8Br-cAMP) were studied for their effects on transepithelial water flux in toad urinary bladder. Arginine vasopressin, arginine vasotocin, oxytocin, desamino-8-D arginine vasopressin, forskolin and 8Br-cAMP stimulated hydro-osmotic water flux in a dose-dependent fashion. The rank order of potency was arginine vasotocin greater than arginine vasopressin greater than oxytocin greater than desamino-8-D-arginine vasopressin greater than forskolin greater than 8Br-cAMP. The vasopressin analogs [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine,8-arginine]vasopressin (SK&F 100273), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine,4-valine,8-arginine]vasopressin (SK&F 100501), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-D-tyrosine,4-valine,8-arginine]vasopressin (SK&F 100885), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-ethyl)tyrosine,4-valine,8-arginine]vasopressin (SK&F 100398), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-D-isoleucine,4-valine,8-arginine]vasopressin (SK&F 101485), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-ethyl)-tyrosine,4-valine,8-arginine]vasopressin (SK&F 101498), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-ethyl)D-tyrosine,4-valine,8-arginine,9-desglycine]vasop ressin (SK&F 101926) and [1-(beta-mercapto-beta-beta-cyclopentamethylene propionic acid),2-D-phenylalanine,4-valine,8-arginine] vasopressin (SK&F 101071) antagonized arginine vasopressin-stimulated water flux and displaced the agonist dose-response relationship to the right in a parallel fashion. The most potent antagonists were those having the (O-ethyl)-D-tyrosine substitution at position 2. None of the antagonists tested had any effect on 8Br-cAMP-stimulated water flux at concentrations up to 10(-6)M.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of action and structural requirements of vasopressin analog inhibition of transepithelial water flux in toad urinary bladder. 309 Feb 34

Normal corpus luteum function is determined by function in the follicular as well as the luteal phase. In the follicular phase adequate follicle-stimulating hormone (FSH) and oestrogen stimulation are required for granulosa cell mitosis and luteinizing hormone (LH) receptor synthesis. An increase in LH pulse frequency may also be necessary for adequate oestrogen synthesis and preparation of follicular cells for luteinization and secretion of progesterone. The nature of LH release may also influence luteal function and pre-ovulatory progesterone may increase the responsiveness of the follicle to gonadotrophins. The thecal vascular network becomes extensive around pre-ovulatory follicles and may influence access of gonadotrophins and/or the ability of follicular cells to respond to them. Further vascularization is an early feature of luteinization. Angiogenic factors are found in luteal tissue and prostacyclin increases luteal blood flow. The corpus luteum consists of large cells which secrete most of the progesterone and have prostaglandin F2 alpha receptors and small cells which are responsive to LH. In the luteal phase subnormal luteal function has not been associated with a reduction in LH concentration, pulse frequency or amplitude. The number and occupancy of LH receptors and adenylate cyclase activity do not appear to be altered by a reduction in luteal function. Low density lipoprotein provides the substrate and somatomedin C modulates among other hormones' influences, progesterone production. In addition to the cAMP second messenger system phosphatidyl inositol metabolism may also be associated with LH stimulation. Luteolysis is an active process; prostaglandin F2 alpha or lipoxygenase products and possibly an endogenous GnRH-like ovarian hormone may mediate it as also may oxytocin in some species.
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PMID:The corpus luteum. 328 62

The dose and time treatment effects of arginine vasopressin (AVP) on basal and hCG-stimulated testosterone accumulation by purified mouse Leydig cells in primary culture were examined. Pretreatment for 24 h of Leydig cells with AVP caused a stimulation of the acute (3 h) basal testosterone accumulation. In these conditions, progesterone accumulation was also increased. The stimulatory effect of AVP (10(-11)-10(-5) M) on testosterone accumulation was dose-dependent and as little as 10(-11) M-AVP caused significant stimulation whilst maximal effect was achieved with 10(-7) M. Oxytocin (10(-6) M) also showed a stimulation of testosterone accumulation in basal conditions, but the other peptides tested at the same concentration (neurotensin, somatostatin and substance P) did not have any effect. When Leydig cells were exposed to AVP for a longer period (48 or 72 h), the increase in basal testosterone accumulation disappeared. AVP treatment of Leydig cells for 72 h led to a significant and dose-dependent reduction in the hCG-responsiveness without altering the slope of the hCG dose-response curve. This inhibitory effect, which was also observed when AVP-pretreated Leydig cells were acutely challenged for 3 h with 8-bromo-cAMP, was accompanied by a concomitant increase in progesterone accumulation. These results indicate that AVP can exert a dual effect on mouse Leydig cells: stimulatory on basal testosterone accumulation during short-term exposure (24 h) and inhibitory on the response to hCG stimulation after long-term treatment (72 h). They provide additional evidence that neurohypophysial peptides directly affect Leydig cell steroidogenesis.
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PMID:Time-related effects of arginine vasopressin on steroidogenesis in cultured mouse Leydig cells. 333 82

The in vitro spontaneous isometric-developed tension (IDT) of uterine horns obtained from diestrous rats exhibited, after 60 min of post-isolation activity, a clear decrease in magnitude, averaging 18.2 +/- 5.2%. In presence of tolbutamide, a concentration-dependent decrease of IDT, significantly greater than the spontaneous reduction (75.1 +/- 5.4%, with tolbutamide at 10(-4) M), was observed. Incubation with propranolol (10(-6) M) or with sotalol (10(-4) M) failed to alter the negative inotropism evoked by tolbutamide. On the other hand, the sulfonylurea (10(-4) M) shifted most points of the dose-response curve to the right for the contractile stimulation elicited by oxytocin, an influence not altered by the simultaneous presence of propranolol or sotalol. Tolbutamide failed to influence the negative inotropic dose-response curve for isoproterenol and did not modify the decrease in contractions evoked by theophylline (10(-4) M). It was also found that tolbutamide was devoid of action on the basal release of prostaglandin E2 from uterine strips and on the positive inotropic dose-response curve for added PGE2 or PGF2 alpha, constructed in presence of indomethacin (5 X 10(-6) M). The present findings do not permit a simple explanation regarding possible factors underlying the negative uterine inotropic influence of tolbutamide in the rat uterus. However, it appears that alterations in the integrity of tissue excitability and contractile apparatus, adrenergic implications, changes in uterine cAMP levels, inhibition of cyclo-oxygenase or low PEG2 synthesis and release, are not plausible mechanisms to explain the negative inotropism of tolbutamide. Therefore, it is suggested that the contractile depression evoked by tolbutamide and its action on the contractile effect of oxytocin might be linked to the impaired synthesis of other prostanoids, namely PGF2 alpha, PGI2 or PGD2, although the participation of not yet determined factor(s), namely changes in Ca2+ ion movements, cannot be discarded.
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PMID:Tolbutamide in vitro diminishes spontaneous and oxytocin-induced contractions of uterine smooth muscle from diestrous rats. 348 42

The effects of rat CRF, arginine vasopressin (VP), oxytocin (OXY), and isoproterenol (ISO) on the biosynthesis and release of pro-ACTH/endorphin-derived peptides by monolayer cultures of rat anterior pituitary cells in complete serum-free medium (CSFM) were studied. When cells were exposed to hormone for 3 h, CRF, VP, OXY, and ISO were each able to stimulate secretion of immunoactive hormone into culture medium. To determine the effects of chronic secretagogue exposure on corticotrope function, cultures were exposed to hormone for 14 days, and total hormone production was measured by immunoassay (cumulative hormone secreted plus cell hormone content). In the absence of CRF, total hormone production increased 3.6 +/- 0.2-fold (mean +/- SEM) over the period from 2-14 days; chronic CRF treatment brought about a 7.9 +/- 0.7-fold increase in total hormone production over the same period (P less than 0.0025) or a 2.2-fold increase over control cells. Total hormone production was not affected by chronic treatment with VP (100 nM), OXY (100 nM), or ISO (100 nM); the response of the cells to chronic CRF treatment was unaltered by chronic inclusion of VP, OXY, or ISO. To examine the chronic effects of secretagogues more directly, anterior pituitary cells were grown in control CSFM or in CSFM containing CRF or VP for 7 days and then incubated in medium containing radiolabeled amino acid for 15 min. The newly synthesized pro-ACTH/endorphin was quantified by immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Cells grown in CSFM containing CRF synthesized 1.9 times more labeled pro-ACTH/endorphin that cells grown in control CSFM or in CSFM containing VP. Chronic exposure of anterior pituitary cultures to 8-bromo-cAMP stimulated both synthesis and release of pro-ACTH/endorphin-derived peptides, suggesting that a secretagogue capable of producing a sustained elevation in intracellular cAMP levels will stimulate prohormone synthesis.
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PMID:Effect of chronic secretagogue exposure on pro-adrenocorticotropin/endorphin production and secretion in primary cultures of rat anterior pituitary. 349 70

A possible role for adenylcyclase in insulin secretion was investigated. Isoproterenol, a predominantly beta-adrenergic agent, when mixed with an alpha-adrenergic blocking agent (phenoxybenzamine), stimulated insulin secretion from pieces of the rat's pancreas in vitro. Theophylline, caffeine, 3'5'-cyclic AMP, glucagon, adrenocorticotropin (ACTH), and thyrotropin (TSH), all of which are thought to act through the adenylcyclase systems in the liver and adipose tissue, also stimulated insulin secretion in vitro; oxytocin and vasopressin, which do not stimulate lipolysis in adipose tissue, were inactive. In all cases, stimulation of insulin secretion could not be detected when glucose was absent or present in only low concentrations (less than 100 mg/100 ml) and was maximal at high levels of glucose (300 mg/100 ml). When pancreatic tissue was obtained from normoglycemic rats and contained no detectable glycogen in the Islets, the stimulant effects of glucose and of theophylline were reduced or abolished by mannoheptulose and 2-deoxyglucose. When tissue was derived from rats infused for 8-10 hr with glucose and contained glycogen, theophylline, even in the absence of glucose, stimulated secretion and this effect was reduced by 2-deoxyglucose but not by mannoheptulose. It is suggested that the beta-cell contains an adenylcyclase system through which phosphorylase and possibly phosphofructokinase could be activated; and that insulin secretion could depend upon and be regulated by hormones and other substances which influence the rate at which glycolysis proceeds within the beta-cell.
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PMID:A possible role for the adenylcyclase system in insulin secretion. 429 54

The isolated urinary bladder of the toad responds to neurohypophyseal hormone with a net increase of water transport from the mucosal to the serosal solution in the presence of an osmotic gradient. This response is mediated intracellularly by cyclic 3',5'-adenosine monophosphate (AMP). The present study demonstrates that hydroosmotically active substances such as oxytocin, dibutyryl cyclic 3',5'-AMP, and theophylline, but not hydroosmotically inactive substances, induce the uptake of horseradish peroxidase from the mucosal solution. Peroxidase taken up by the mucosal cells is demonstrable in small tubules and vesicles, and eventually accumulates in lysosomes. The uptake of peroxidase from the serosal solution into similar bodies in the mucosal cells is not hormone-dependent. It is also shown that peroxidase does not penetrate the tight junction from either the mucosal or serosal solution. These results extend previous findings which implicated the apical membrane of the mucosal epithelium as the site affected by neurohypophyseal hormones. A mechanism based on secretory phenomena is proposed as a framework for future investigations of apical membrane permeability changes and pinocytosis.
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PMID:Correlation between pinocytosis and hydroosmosis induced by neurohypophyseal hormones and mediated by adenosine 3',5'-cyclic monophosphate. 432 55

The effects of oxytocin upon tissue cAMP content and short-circuit current (SCC) were measured in the urinary bladder of the toad, Bufo marinus. Tissue cAMP levels doubled before any increment in SCC was observed, the two hormone responses were quantitatively related, and a threshold level for an effect of cAMP upon sodium transport was demonstrated. The period of time over which cAMP levels continued to rise after the threshold level had been attained seemed invariant with hormone concentration. The rate at which cAMP levels rose increased with hormone concentration yielding hormone concentration-dependent maximal levels. The decay of cAMP levels was delayed when sodium influx was curtailed, suggesting a sodium-regulatory effect upon tissue cAMP levels.
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PMID:Cyclic AMP and sodium transport. Quantitative and temporal relationships in toad urinary bladder. 435 77

Enzymically dispersed luteal cells obtained from PMSG-hCG-treated immature pseudopregnant rats were incubated with oxytocin and vasopressin. In response to increasing doses of hCG the rat luteal cells produced progesterone and accumulated intracellular cAMP in a dose-dependent manner. A neuropeptide GnRH agonist (4 X 10(-6) M) produced a significant inhibition of hCG-stimulated progesterone production and of accumulation of intracellular cAMP. However, neither the basal nor the hCG-stimulated rate of progesterone production and level of intracellular cAMP was affected by the neurohypophysial peptides tested. Therefore, it is concluded that oxytocin and vasopressin do not have a direct action on steroidogenesis by rat luteal cells.
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PMID:Oxytocin and vasopressin have no effect on progesterone production and cyclic AMP accumulation by rat luteal cells in vitro. 608 69

In the present work an attempt is made to get a deeper insight into the mechanism of labor and the events leading to the onset of labor by means of radioimmunological measurements of OT, PGE, PGF, PGEM and PGFM and by determining the oxytocin sensitivity and the concentration of oxytocin receptors. Prostaglandins play a major role for the mechanism of labor in labor of spontaneous onset as well as in several forms of induced labor (intravenous infusion of OT, amniotomy, local application of PGE2). The reason for this seems to be the 3 fold action of prostaglandins: stimulation of myometrial contractions, cervical softening, induction of gap junctions. Moreover prostaglandins produced in the placenta play a major role in the mechanism of placental separation and expulsion. Oxytocin seems to be of importance for the initiation of labor and the final expulsion of the fetus. Immediately before the onset of regular contractions a marked increase of oxytocin sensitivity can be demonstrated which correlates very well with an increase of oxytocin receptor concentration in the myometrium and decidua. Due to this increase in oxytocin sensitivity no rise in oxytocin plasma levels is necessary to induce labor. Apart from the induction of myometrial contractions oxytocin leads via receptors in the decidua to a stimulation of prostaglandin synthesis which can also be demonstrated in vitro. In cases of premature contractions the same mechanisms seem to be operational as at term, oxytocin and prostaglandins again playing a major role. Inhibition of contractions with ethanol is based on the capacity of alcohol to inhibit oxytocin secretion. The contractions inhibiting effect of ritodrine is mediated through the cAMP induced relaxation of the myometrium although possibly a direct reduction of prostaglandin synthesis by ritodrine is possible. Increasing estrogen and decreasing progesterone activities at term lead to multiple subtile changes leading to an increased prostaglandin synthesis and mainly to a rise in oxytocin receptor concentration in the myometrium and the decidua. Oxytocin from the fetal and maternal side stimulates contractions in the myometrium and prostaglandin synthesis in the decidua leading to the onset of labor. With progressing cervical dilatation prostaglandin synthesis is further stimulated; these prostaglandins together with the increased oxytocin plasma levels in the second stage of labor lead to expulsion of the fetus. After delivery prostaglandin synthesis in the placenta leads to placental separation and expulsion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The importance of oxytocin and prostaglandins to the mechanism of labor in humans]. 609 5


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