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)

Homogenates of human luteal tissue bound radioiodinated luteinizing hormone releasing hormone agonist. Specific binding was both time- and temperature-dependent. Native LHRH and two LHRH agonists competed for binding, whereas TRH, somatostatin and oxytocin did not, indicating that the binding sites were specific. The apparent Ka values were 2 X 10(7)M-1 for both LHRH agonists and 10(6)M-1 for native LHRH. This is the first demonstration of specific binding of LHRH to human ovarian tissue. No binding could be detected to ovarian tissue from postmenopausal women.
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PMID:Specific binding of luteinizing hormone releasing hormone to human luteal tissue. 630 78

Partially purified cell membranes were prepared from midterm and term placentas after sedimentation on a sucrose density gradient. Biochemical characterization showed that the sucrose density pellet was enriched 8-fold in alkaline phosphatase activity and also contained the majority of [125I]LHRH binding sites. This enrichment was also confirmed by electron microscopy. Specific binding of LHRH was then determined by incubating iodinated LHRH or two of its superanalogs with increasing doses of the corresponding radioinert ligand. Scatchard representation of the data showed curvilinear plots whose first component revealed, for both stages of pregnancy, saturable binding of [125I]LHRH and its agonists with similar association constants (Ka) that ranged between 5.5 X 10(5) M-1 and 1.1 X 10(7) M-1. When standardized per milligram of DNA content, the number of binding sites ranged between 225 and 310 X 10(-12) M. Specificity was evidenced by the inability of a biologically active LHRH antagonist, oxytocin, and TRH to inhibit [125I]LHRH binding. Short term placental cultures incubated with 1.5 X 10(-6)M LHRH had increased production rates of both immunoassayable and bioassayable hCG, and this effect was 4-fold higher in midterm placental cultures. Placental incubations with either buffer or equimolar concentrations of oxytocin or TRH had no effect on hCG production. These observations expand information on extrapituitary binding sites of LHRH and suggest a role for this peptide in the physiology of the human placenta.
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PMID:Luteinizing hormone-releasing hormone binds to enriched human placental membranes and stimulates in vitro the synthesis of bioactive human chorionic gonadotropin. 632 54

To determine whether oxytocin (OT) could alter the release of PRL and other hormones from the anterior pituitary gland, the effects of OT were examined in two in vitro and two in vivo test systems. Cells dispersed from anterior pituitary glands of intact adult male rats were incubated in medium containing OT at doses of 10(-8), 10(-7), 10(-6), and 10(-5) M in two trials. OT stimulated PRL release 1.5-fold (P less than 0.01) and 2- to 3-fold (P less than 0.001) above control levels at 10(-8) and 10(-7) M doses, respectively, thus indicating a dose-dependent relationship. Higher doses did not produce a further elevation above that obtained with 10(-7) M OT. Arginine vasopressin (AVP) caused a slight decrease in PRL release from dispersed cells while TRH produced a small (25%), significant, but nondose-related increase in PRL release. Hemipituitary glands from adult male rats, incubated with 10(-6) and 10(-5) M OT, released twice as much PRL (P less than 0.01) into the medium as paired controls, but 10(-7) M OT was ineffective. The iv injection of 1 or 10 micrograms OT into conscious male rats elevated plasma PRL by 50% (P less than 0.05) or 500% (P less than 0.001), respectively, above basal values at 5 min only. Vehicle or 0.1 microgram OT were without effect. When 0.1 microgram OT was microinjected into the third ventricle (3V) of conscious male rats, it paradoxically reduced plasma PRL by 40% at 30 min (P less than 0.05), whereas 1 microgram OT significantly lowered PRL at 5-60 min, with the maximum suppression (60%, P less than 0.001) occurring at 30 min. These latter findings may indicate that an ultrashort loop feedback mechanism exists whereby exogenous OT decreases hypothalamic OT secretion, thereby reducing the OT stimulus for PRL release. The specificity of the OT effect on PRL was attested to by the failure of OT to alter significantly FSH, LH, and TSH in each system. GH was unchanged except that 3V-injected OT (1 microgram only) elevated (P less than 0.001) plasma GH at 15-30 min. These results support the view that OT acts directly on the cells of the anterior pituitary gland at low to high doses to release PRL specifically and in a dose-related fashion. In contrast, 3V injection of OT reduces PRL secretion, thereby suggesting that OT may decrease its own neurosecretion by ultrashort loop feedback and thus reduce an OT stimulus for PRL release.
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PMID:Hypothalamic and pituitary sites of action of oxytocin to alter prolactin secretion in the rat. 640 33

Immunohistochemical studies on cholecystokinin-like (CCK-ir) substances in colchicine-pretreated rats demonstrated that in addition to CCK-ir cells in the magnocellular portion of the paraventricular nucleus. CCK-ir cells are also present among the parvocellular neurons. Radioimmunoassay of CCK after paraventricular lesions indicate that most, if not all, of the CCK in the posterior pituitary and in the median eminence originates from the paraventricular nucleus. It appears that CCK-fibers, like other neuropeptidergic fibers from the paraventricular nucleus (vasopressin, oxytocin, TRH, CRF) enter the medial basal hypothalamus through a common gate--the lateral retrochiasmatic area--in traveling to the median eminence.
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PMID:Cholecystokinin in the hypothalamo-hypophyseal system. 672 68

We have compared the effectiveness of TRH and a rat hypothalamic PRL-releasing factor (PRF; previously incubated with rat serum to destroy TRH) in stimulating the release of PRL into the plasma of conscious lactating rats when injected before and after pituitary PRL had been depleted and transformed into releasable PRL by 10 min of suckling. TRH (1.25 microgramsss) and PRF [equivalent to 2.5 stalk median eminence (SME) fragments] each caused a small increase (38 and 30 ng, respectively) in the plasma PRL concentration within 10 min when injected into nondepleted mothers. The levels then fell quickly. Suckling, by comparison, caused a sustained 175 ng/ml increase above basal levels. Though PRL depletion occurred, as expected, as a result of suckling, there was no measurable depletion within the pituitaries of TRH- or PRF-injected rats. By contrast, the iv administration of TRH (doses ranging from 2-250 ng) and hypothalamic PRF (doses ranging from 0.2-1.0 SME equivalent) after depletion-transformation had been effected by 10 min of suckling resulted in a rapid and, in most instances, a sustained elevation in the plasma PRL concentration comparable to that seen after suckling. Dose-response relationships, though, were not clearly evident with either PRF or TRH. Neither saline, 1.25 microgram TRH previously incubated in serum, 50 mU oxytocin, 1 microgram dopamine, 25 microgram LHRH, nor an extract of cerebral cortex prepared in the same manner as hypothalamic TRH caused plasma PRL to rise after PRL depletion. We conclude that TRH and possibly a separate hypothalamic PRF have a stimulatory action upon the releasable, but not upon the depletion-transformation, phase of PRL secretion in the lactating rat.
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PMID:Evidence that thyrotropin-releasing hormone and a hypothalamic prolactin-releasing factor may function in the release of prolactin in the lactating rat. 677 47

By radioimmunoassay and immunocytochemical techniques, 14 neuropeptides have been measured and localized in the rat median eminence. Neuropeptides with inhibitory or stimulatory effects on the anterior pituitary hormones as well as posterior pituitary hormones are present in the median eminence in the highest concentrations of the central nervous system. All these peptides (LH-RH, TRH, somatostatin, CRF, vasopressin, oxytocin) are of preoptic or hypothalamic origin and they are transported to the median eminence by loop-like fiber systems through the lateral retrochiasmatic area. Within the median eminence, the pericapillary space constitutes the main common pathway. Three major transport routes--axons, vessels, liquor spaces--are separated from each others by only basement membranes, which allow free communications downwards to the pituitary but also backwards to the central nervous system.
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PMID:Neuropeptides in the median eminence: their sources and destinations. 681 29

Targeted tumorigenesis, using the POMC gene promoter ligated to the simian virus 40 large T antigen, generated transgenic mice with massive tumors of the intermediate lobe (IL) of the pituitary. Inoculation of nude mice with the IL tumor cells resulted in very large secondary tumors. As the IL from several species produces a potent PRL-releasing factor (PRF), it was of interest to determine whether IL tumors from these mice also contain PRF. The objectives were to 1) measure serum PRL levels in mice with IL tumors, 2) determine whether these tumors contain PRF and examine its chromatographic properties, and 3) analyze whether this PRF is related to POMC, its derivatives, or other PRL secretagogues. Serum PRL levels were 5- to 6-fold higher in transgenic than in control mice. Primary and secondary IL tumors were acid extracted and successively fractionated using Sephadex G-100 gel filtration and reverse phase and gel permeation HPLC. PRF activity was determined using short term incubation of tissue extracts or column fractions with GH3 cells. Crude tumor extracts exhibited a strong and dose-dependent PRF activity. Upon chromatography, the PRF activity from either primary or secondary tumors resolved into two classes of compounds: a big PRF with an estimated mol wt of 70-80 kilodaltons and two small, very hydrophobic peptides. The elution profiles of the three PRFs differed from those of beta-endorphin, alpha MSH, beta MSH, ACTH, TRH, oxytocin, angiotensin II, vasoactive intestinal polypeptide, or corticotropin-like intermediate peptide. In summary, we have identified an animal model with IL tumors that has hyperprolactinemia and overproduces PRF. Two classes of PRFs, big and small, were resolved which differ from POMC derivatives and known regulators of PRL release. These data suggest that PRF is produced by melanotrophs, but is not a product of the POMC gene. The IL tumors should provide an excellent source for the purification and structural elucidation of PRFs.
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PMID:Identification of two classes of prolactin-releasing factors in intermediate lobe tumors from transgenic mice. 778 36

Acting in vivo, adrenalin and noradrenalin cause a statistically significant and permanent decrease in the motility of mouse spermatozoa remaining in the vas deferens. Intratesticular injection of vasopressin, oxytocin, insulin, and glucagon results in a decrease in spermatozoa motility in vas deferens, removal the spermatozoa to PBS in vitro, and an increase in percentage of motile spermatozoa on incubation medium. Thyroxine, calcytonin, and TRH did not affect motility of mouse spermatozoa in vivo.
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PMID:Effects of selected hormones on the motility of spermatozoa in the mouse vas deferens. 785 64

Oxytocin (OT) and arginine vasopressin (AVP) have been reported to release PRL both in vivo and in vitro. The objectives of this study were 1) to compare the potencies of the PRL-releasing activities of OT and TRH using cultured anterior pituitary (AP) cells, and 2) to assess the PRL-releasing activity of naturally occurring neurohypophysial hormones and selected analogs. AP cells were incubated with peptides for 15 min, and medium PRL concentrations were determined by enzyme-linked immunosorbent assay. OT at 25, 100, and 400 nM increased PRL release by 110%, 175%, and 270%, respectively; higher concentrations (1600 and 6400 nM) did not cause a further increase in PRL release. TRH was 5-10 times more potent than OT on a molar basis. GH3 cells, a somatommamotroph tumor cell line, did not respond to OT and related compounds, but showed a similar responsiveness to TRH as AP cells. Twelve neurohypophysial peptides and selected analogs were incubated with AP cells, and their relative PRL-releasing activities were compared. OT and arginine vasotocin (AVT) showed the highest PRL-releasing activity. T4-G7-oxytocin, mesotocin, isotocin, lysine vasotocin, and AVP showed a moderate PRL-releasing activity, whereas, lysine vasopressin, desmopressin, tocinoic acid, pressinoic acid, and oxytocin free acid showed very low or no PRL-releasing activity. Coincubation of OT, AVT, or AVP with a specific OT receptor antagonist abolished their PRL-releasing activity. We conclude that 1) OT and related peptides are capable of stimulating PRL release in vitro, but their potencies are significantly lower than that of TRH; 2) unlike primary AP cells, GH3 cells are unresponsive to OT and related peptides; 3) AVT and AVP probably stimulate PRL release by acting via an OT receptor; and 4) the amino acid residues in positions 3 and 8 in the peptide chain and an amidated C-terminus are critical for the PRL-releasing activity of the neurohypophysial peptides.
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PMID:Prolactin-releasing activity of neurohypophysial hormones: structure-function relationship. 827 25

Data available in the literature and the author's own findings of the effects of regulatory peptide (RP) and their analogues are summarized. MIF, TRH, and its analog PR-546, the paraopioid RP, leuenkephalin, dalargin, the ACTH analogue Semax, tafcin, thymosine, interleukin-1, vasopressin, oxytocin, bradykinin, defencin, and some proline-containing oligopeptides, such as Pro-Gly, Gly-Pro, Trp-Pro, Pro-Gly-Pro, Gly-Pro-Gly-Gly were studied. A complex of in vitro and in vivo tests identified three groups of RP: 1) neutral ones as to the hemostatic reactions studied; 2) stimulants of hypercoagulation and fibrin polymerization; 3) inhibitors of blood coagulation, increased fibrinolysis, and fibrin demopolymerization. The fibrinolytic and antithrombotic effects of Semax (in vivo), the procoagulative action of defencin, and the enhanced anticoagulant effects in the combinations of Semax-heparin and tafcin (in vivo) attract particular attention. Semax alone and in combination with heparin is recommended for clinical studies in respective hemostatic abnormalities.
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PMID:[The modulation of hemostatic reactions in vitro and in vivo by representatives of regulatory peptide families]. 892 38


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