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)

Systematic analysis of the hydrolysis of benzyloxycarbonyl (Cbz)-dipeptides by cathepsin A [EC 3.4.12.1] purified from rat liver lysosomes showed that multiple forms of cathepsin A preferentially cleave peptide bonds with leucine, methionine, and phenylalanine. Cbz-Met-Met, -Met-Phe, -Phe-Met, and -Phe-Ala were hydrolyzed 6 to 8 times faster than the standard substrates, Cbz-Glu-Phe and Cbz-Glu-Tyr. The pH optima of the hydrolyses were 4.6 to 5.8. Hydrolysis of peptide bonds with glycine, isoleucine, and proline was very slow, but the rate depended on the nature of the adjacent amino acids. Proteins such as albumin, cytochrome c, gamma-globulin, hemoglobin, histone, myoglobin, and myosin were scarecely degraded. Peptide hormones, such as glucagon and adrenocorticotropic hormone (ACTH) were hydrolyzed markedly with optimum pH's of 4.5 and 4.6, respectively. Angiotensin I, II, bradykinin, Lys- and Met-Lysbradykinin (kallidin and Met-kallidin), and substance P were also hydrolyzed at appreciable rates. pH optima for these peptide hormones were 5.2 to 5.6. On the other hand, insulin and its A chain, luteinizing hormone-releasing hormone (LH-RH), oxytocin and vasopressin were cleaved slowly. In the hydrolyses of glucagon and other peptides, multiple forms of rat liver lysosomal cathepsin A again showed a carboxypeptidase nature, cleaving peptide bonds sequentially from the carboxyl terminal. Almost all of the amino acids were cleaved on prolonged incubation. Vaso-activites of angiotensin II and bradykinin were rapidly lost on hydrolysis by cathepsin A. Lysosomal cathepsin C [dipeptidylaminopeptidase I, EC 3.4.14.1] also activated angiotensin II, but did not inactive bradykinin. Cathepsin A, therefore, can be regarded as one of the lysosomal angiotensinases and kinases. No distinct differences were observed between the multiple forms of cathepsin A in these hydrolyses and inactivations of peptides.
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PMID:Studies on cathepsins of rat liver lysosomes. III. Hydrolysis of peptides, and inactivation of angiotensin and bradykinin by cathepsin A. 1 61

Rabbits were anesthetized with urethane, and the concentration of 3',5' cyclic adenosine monophosphate (cAMP) in cerebrospinal fluid (CSF) was measured before and after injection into the cisterna magna of the following biologically active peptides and amines; adrenocorticotropin (ACTH), beta-melanocyte-stimulating hormone (beta-MSH), choroid plexus peptide IIF, arginine vasopressin, oxytocin, glucagon, epinephrine, serotonin, histamine, and acetylcholine. Only epinephrine and the lipolytic-melanotropic peptides ACTH, beta-MSH, and IIF influenced cAMP. Five to 500 mug ACTH caused a 3 to 10X increase in cAMP within 30 min; the concentration of nucleotide returned to baseline within 60-90 min after 5 or 50 mug, and remained elevated for at least 120 min after 500 mug. Effects of the same magnitude and tempo as those caused by 5 to 500 mug ACTH were produced by .1 to 10 mug beta-MSH and 5 to 500 mug IIF. Epinephrine at doses of 5 to 500 mug caused rises in cAMP of similar degree as the same dose of ACTH or peptide IIF, but the peak value was not reached until 60 to 90 min after injection.
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PMID:Effect of intrathecal injection of melanotropic-lipolytic peptides on the concentration of 3',5' cyclic adenosine monophosphate in cerebrospinal fluid. 17 24

Transitional epithelium lining rabbit urinary bladders was isolated and studied in vitro. The homogeneity of the isolated epithelium was demonstrated by light and electron microscopical monitoring as well as cell culture studies. Transitional epithelium responded to epinephrine and prostaglandin E1 (PGE1) in the presence of 2mM 1-methyl, 3-isobutylxanthine (MIX) with increases in intracellular levels of cyclic adenosine 3':5'-monophosphate (cyclic AMP). Corticotropin, aldosterone, insulin, parathyroid hormone and vasopressin were slightly but significantly stimulatory under similar conditions. Glucagon and oxytocin were not stimulatory at the concentrations tested. The effects of epinephrine and PGE1 were potentiated by 2mM MIX 20-fold or greater. The cells were slightly more sensitive to PGE1 then to epinephrine. The prostaglandin produced a noticeable response at about 10nM, while effects of epinephrine were discernible at 0.1muM. Maximal responses to both effectors were seen at about 10muM. The action of 10muM epinephrine, but not 10muM PGE1, was completely abolished by 0.1mM propranolol. Responses to combinations of epinephrine and PGE1 were additive. Cyclic AMP accumulated in the incubation medium of transitional epithelial cells exposed to epinephrine, PGE1, MIX, or combinations of the agonists. The appearance of cyclic AMP in the medium was slow compared to the rate of intracellular accumulation, but reached significant levels following prolonged stimulation.
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PMID:The effects of hormones on cyclic adenosine 3':5'-monophosphate accumulation in transitional epithelium of the urinary bladder. 17 60

Rabbits were anesthetized with urethane and were given intracisternal injections of the following substances: adrenocorticotropin, beta-melanocyte stimulating hormone, choroid plexus peptide IIF, epinephrine, serotonin, histamine, oxytocin, lysine and a arginine vasopressins, acetylcholine and melatonin. The effects on the concentration of 3', 5' cyclic guanosine monophosphate (cGMP) in cerebrospinal fluid were then measured. Only melatonin and acetylcholine caused a significant (p less than 0.05) effect on cGMP concentration. Both agents increased the nucleotide's concentration within 30 min. Melatonin was about 1,000 times more potent than acetylcholine; the mininal effective doses were 1 mug and 1,000 mug, respectively.
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PMID:Injection of melatonin into cisterna magna increases concentration of 3', 5' cyclic guanosine monophosphate in cerebrospinal fluid. 18 65

Choroid plexus of rabbit and rat was incubated for 2-30 min at 37 degrees C under 95% O2-5% CO2 in Tyrode solution containing 10 mM glucose and 1 mM theophylline with these agents: epinephrine, norepinephrine, isoproterenol, dopamine, histamine, serotonin, arginine, and lysine vasopressins, oxytocin, angiotensin, adrenocorticotropin (ACTH), beta-melanocyte-stimulating hormone, and choroid plexus peptide IIF. After incubation, tissue and medium were analyzed for 3', 5' -cyclic adenosine monophosphate (cAMP) content. Each amine or peptide was tested initially at 1,000 microng/ml. Only ACTH and serotonin affected cAMP content of rabbit choroid plexus. At 1,000 microng/ml, these agents caused a 10 and 4 times (respectively) increase in cAMP content of tissue + medium at 2-10 min with decline in content at 10-30 min. More than 90% of the increment was located in tissue, less than 10% in medium. Minimal effective dose (MED) to cause a significant (P less than .05) accumulation of cAMP was 0.1 microng/ml (2.2 x 10(-8) M) for ACTH and 10 microng/ml (5.7 x10(-3) M) for serotonin. Only isoproterenol, epinephrine, and norepinephrine influenced cAMP content of rat choroid plexus. MED's for this effect by isoproterenol, epinephrine, and norepinephrine were .001, .01, and 10 microng/ml (4.7 x 10(-9), 5.5 x 10(-8), and 5.9 x 10(-5) M), respectively.
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PMID:Effects of hormones on 3', 5' -cyclic adenosine monophosphate in choroid plexus. 19 84

Evidence is presented for a number of events in the fetal hypothalamic-pituitary axis which may play a key role in the onset of labour: (1) In the sheep fetus a progressive rise in the fetal circulating concentrations of corticotropin in the days preceding delivery; (2) In the human fetus a switch from the production of corticotropin-like fragments (melanotropin and corticotropin-like intermediate lobe peptide) to authentic corticotropin in the last weeks of gestation; there is evidence also for a placental origin of corticotropin; (3) In the human fetus, a release of oxytocin and vasopressin associated with the process of spontaneous labour.
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PMID:The fetal hypothalamus and pituitary in the initiation of labour. 20 96

Parturition in sheep is initiated by a sharp rise in the rate of secretion of cortisol by the fetal adrenal. Increased secretion is due partly to enhanced responsiveness to corticotropin (ACTH) and partly to increased fetal concentrations of corticotropin. Cortisol acts on placental enzymes active in the biosynthesis of oestrogens from progesterone. Thus placental secretion of oestrogen increases and that of progesterone decreases. This change in the ratio of oestrogen: progesterone, particularly the rise in oestrogen, stimulates release of prostaglandin F2alpha (PGF2alpha) from the maternal placenta and to a lesser extent from the myometrium. PGF2alpha enhances the myometrial response to oxytocin and, after a latent period, stimulates contractions. The onset of parturition is normally associated with softening of the cervix, the mechanism of which is uncertain. Uterine contractions in the presence of a distensible cervix lead to parturition.
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PMID:Parturition in the sheep. 20 98

In rat hypothalamus intraventricularly injected with colchicine, the same neurons of the ventral region are stained with I.S. against alpha and beta-endorphin, (1-24) and (17-39) ACTH, alpha and beta-MSH, and beta-LPH. They are distinct from those producing LH-RH, somatostatin, neurophysin, and dopamine. These results suggest that the same neurons elaborate peptides identical with or immunologically related to endorphins, ACTH, alpha-MSH and beta-LPH, probably issued from a common precursor.
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PMID:[Immunocytologic analysis, in rat hypothalamus, of neurons producing peptides related to endorphin, ACTH, MSH and beta-LPH. Comparison with other peptidergic and monoaminergic neurons]. 23 Aug 87

In rat brains intraventricularly injected with colchicine, the same discrete neurons of the arcuate and ventromedial nuclei can be stained with antisera against alpha- and beta-endorphins, (1-24)ACTH, (17-39)ACTH, alpha- and beta-MSH, and beta-LPH, as demonstrated by comparative studies in consecutive serial sections. These neurons are strongly reactive with anti-(17-39)ACTH, anti-beta-endorphin, anti-alpha-MSH and anti-beta-MSH, and more faintly stained with anti-alpha-endorphin, anti-beta-LPH and anti-(1-24)ACTH. Exceptionally, neurons reactive with anti-(17-39)ACTH and anti-beta-endorphin are poorly stained or completely negative with anti-alpha-MSH and anti-beta-MSH. Immunoreactive fibers end in the lateral median eminence and in the arcuate nucleus proper, or form ascending pathways along the third ventricle. Comparative studies with other antisera or with the Falck and Hillarp technique show that these neurons differ from the elements producing LH-RH, somatostatin, neurophysin, oxytocin, vasopressin and dopamine. These results suggest that the same neurons of the rat hypothalamus synthesize several neuropeptides identical with or immunologically related to endorphins, ACTH, alpha-MSH and beta-LPH, probably arising from a common precursor molecule similar to that found in the corticotropic cells of the pituitary. These neuropeptides of a common cellular and molecular origin might be involved in basic processes of the central nervous system as neurotramsmitters or neuromodulators.
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PMID:Neurons of the rat hypothalamus reactive with antisera against endorphins, ACTH, MSH and beta-LPH. 23 Sep 4

The possibility that the fetal brain or pituitary either initiates parturition or influences the course of labour was studied in human and rat. The results when corticotropin or neurohypophysial hormones were injected directly into human anencephalic fetuses in utero, and data obtained from 147 clinical records of such fetuses, seemed to show that the fetal brain does not trigger the onset of parturition. On the other hand, the course of labour was seriously protracted in anencephalic fetuses. Gestation length of brain-aspirated rat fetuses was not significantly longer than in sham-operated controls. However, the course of labour was protracted in the brain-aspirated fetuses. A similarly protracted expulsion pattern was observed in Brattleboro rats homozygous for a hypothalamic form of diabetes insipidus. These data all pointed to the likelihood that fetal neurohypophysial hormones stimulate the course of labour. Neither oxytocin nor vasopressin could be demonstrated in the rat fetus on the last day of pregnancy, when specific immunofluorescence was used. However, a closely related compound was found that was identified as most probably being vasotocin. The hypothesis is put forward that this fetal hormone normally stimulates the course of labour.
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PMID:The influence of the fetal hypothalamus and pituitary on the onset and course of parturition. 24 94


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