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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Milk-ejection activity was determined in the blood plasma of ewes during normal milking and during milking when adrenaline was injected intravenously before or after udder stimulation. It was found that administration of adrenaline either before or after udder washing, decreased the oxytocin concentration and milk yield but increased the yield by hand-stripping. Adrenaline also retards the average time for peak oxytocin concentration. These results and the use of a beta-receptor blocker to inhibit the effect of adrenaline at the myoepithelial cell level indicate that in ewes adrenaline can prevent the release of oxytocin from neurohypophysis.
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PMID:Inhibitory effect of adrenaline on oxytocin release in the ewe during the milk-ejection reflex. 43

Recent data on various environmental stressors and blood hormone patterns are presented for lactating cattle. Known stressor effects of such factors as environmental temperature, air pollution, and noise on the plasma thyroxine, growth hormone, cortisol, prolactin, progesterone, luteinzing hormone, epinephrine, and norepinephrine of lactating cattle are discussed. Information on stressor effects is lacking on glucagon, insulin, vasopressin, calcitonin, oxytocin, thyrotrophic hormone, follicle stimulating hormone, melatonin, parathyroid hormone, and estrogens in the lactating cow. The importance of evaluating both the effect of environmental stressor and of production or lactation intensity is emphasized in the overall interpretation of changes in hormone of plasma. The short and long term environmental heat effects on thyroxine, cortisol, and growth hormone are clear with initial increased due to acute stressors and a decline of amounts in plasma after prolonged exposure to stressors. The relationship of amounts in plasma of these hormones to milk production appears to be related directly for cortisol, growth hormone, and prolactin with an inverse relationship with thyroxine. Epinephrine and norepinephrine seem to be elevated with prolonged environmental heat stress. However, the influence of intensity of lactation has not been measured. Hormones in plasma as they relate to stressor effects and milk production are important as potential indicators of the physiological state of a cow and reflect the physiological compensations a cow undergoes at various lactation intensities and/or stress exposure.
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PMID:Effects of environmental and other stressors on blood hormone patterns in lactating animals. 98 81

To measure cholinergic, adrenergic and tryptaminergic receptor activity of formaldehyde (HCHO) in rat uterus, albino rats were treated with 5 and 10 mg/kg, ip HCHO for 30 days. Acetylcholine (ACh) in doses 1.33, 2 and 3 micrograms/ml produced mild to moderate contraction of isolated rat uterus in control group. HCHO had no effect on isolated rat uterus per se, however it reduced ACh and carbachol induced contraction and presence of adrenaline influences in respect of ACh and carbachol activity. Adrenaline per se had no effect in control preparations, but reduced carbachol induced contraction. Propranolol had no effect on rat uterus; but its presence in the bathing medium increased activity of adrenaline. 5-Hydroxytryptamine (5-HT) had no effect of its own on isolated rat uterus but its presence in the bathing medium enhanced contractions of carbachol and oxytocin.
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PMID:In vitro study of rat uterus after chronic formaldehyde exposure. 129 16

A microperfusion system was developed to study detailed kinetics of adrenocorticotropic hormone (ACTH) secretion by dispersed rat anterior pituitary cells responding to various ACTH secretagogues. The system approaches hydrodynamics to square-wave stimuli and enables kinetic analysis of ACTH secretion with intervals as short as 5 sec. ACTH secretion initiated within 5 sec of exposure of the cells to corticotropin-releasing factor (CRF), arginine vasopressin (AVP), oxytocin (OT) or angiotensin II (A-II) and reached a maximum within 20-40 sec. CRF induced a plateau-shaped secretion of ACTH which remained constant as long as CRF was perifused. In contrast, the ACTH secretion responding to AVP, OT and A-II rose rapidly to a peak and fell to the baseline despite continued perifusion of these agents. There were two components of ACTH secretory response to AVP and OT. AVP had synergistic effect with CRF only if it was perifused simultaneously with CRF or immediately after CRF was stopped. The ACTH secretory response to A-II was greatly diminished when cells were exposed to AVP or OT before A-II perifusion. Prior exposure to A-II had no effect on the magnitude of the ACTH secretory response to either AVP or OT. Epinephrine, nor-epinephrine, gastrin-releasing peptide, atrial natriuretic factor and cholecystokinin stimulated no significant ACTH secretion in the microperfusion system, although some of them induced ACTH secretion by same cell preparation in static culture systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Physiological analyses of secretory kinetics of adrenocorticotropic hormone (ACTH) from anterior pituitary cells: development and application of a microperfusion system]. 131 80

The ability of de novo biosynthesis of prostaglandins (PGs) in individual whole corpora lutea (CL) obtained from sterile-mated adult pseudopregnant rats on different days of the luteal phase and the post-luteolytic period was evaluated. Production of PGs, progesterone and 20 alpha-dihydroprogesterone were determined after in vitro incubation of CL extirpated from Day 2 to Day 19 after mating. A time-relationship with increased accumulation of PGs in the medium was demonstrated from 18 s to 5 h, with large increments during the first 30 min. Basal accumulation of PGs in the incubation medium was highest for 6-keto-PGF1 alpha (the stable metabolite of prostacyclin) greater than PGE2 greater than PGF2 alpha greater than thromboxane B2 (TXB2) and basal accumulation of PGF2 alpha and PGE2 measured in the medium was maximal on Day 10-11 of pseudopregnancy, concomitantly with a decline in secretion of progesterone. Addition of arachidonic acid (AA) dose-dependently increased synthesis of PGs, with absolute amounts of PGE2 greater than 6-keto-PGF1 alpha greater than PGF2 alpha greater than TXB2 and addition of 14 microM indomethacin markedly inhibited accumulation of all PGs measured. Luteinizing hormone (LH, 10 micrograms/ml) stimulated progesterone secretion on all days during pseudopregnancy, but not on the post-luteolytic Day 19. LH increased PGF2 alpha, PGE2 and 6-keto-PGF1 alpha secretion on Day 13 of pseudopregnancy by 76%, 91% and 28%, respectively, but not on the other days tested. Furthermore, stimulation of PG-synthesis by addition of AA abrogated the LH-induced progesterone accumulation markedly, but only on Day 13 of pseudopregnancy. Epinephrine (5 micrograms/ml) increased production of progesterone and also PGs, but only on Day 2 of pseudopregnancy, whereas oxytocin (100 mIU/ml) was found to be without effect on progesterone as well as PG secretion on all days tested. The results of the present study demonstrates the independent ability of the rat CL to synthesize PGG/PGH2-derived prostaglandins, including the putative luteolysin PGF2 alpha. Secondly, we demonstrate that LH and AA-induced increases in PGF2 alpha and PGE2 production during the luteolytic period, may be an autocrine or paracrine mechanism involved in luteolysis.
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PMID:Synthesis of prostaglandin F2 alpha, E2 and prostacyclin in isolated corpora lutea of adult pseudopregnant rats throughout the luteal life-span. 150 52

Uterine contractions in labour are influenced by endogenous substances such as oestrogens, progesterone, cortisol, oxytocin, prostaglandins, relaxin, adrenergic and cholinergic secretions, cyclic nucleotides and calcium ions. Effects of progesterone and oestrogens are complimentary as well as antagonistic to each other. They regulate formation of gap junctions, influx of calcium ions, synthesis of oxytocin, adrenergic receptors and of prostaglandins and cyclic nucleotides. Cortisol shares a role in a more complex endocrine trigger but is ineffective alone in the initiation of human labour. Adrenaline inhibits and noradrenaline promotes uterine contractions. Cholinergic stimulation increases cyclic GMP promoting uterine contractions. Calcium ions play a key role in uterine contractility. Oxytocin, prostaglandins E and F are powerful stimulants of uterine contractions. Prostaglandins stimulate pregnant uterus from early gestation unlike oxytocin which has little effect in the first and second trimester. They are extensively used for initiating labour and to arrest intractable atonic postpartum haemorrhage. In experiments and in vivo, their effects are modulated by other hormones and substances. With discovery of new drugs, knowledge of how they act on the uterus becomes important. The pharmacology of parturition that may help to understand the interaction of various agents on the pregnant uterus has been discussed.
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PMID:Pharmacology of parturition. 202 68

The effect of manual teat stimulation (milking paradigm) on release of oxytocin, epinephrine and norepinephrine was studied in (1) 15 heifers at 100, 150, 200 and 250 d of gestation and at 30 and 90 d of lactation (during machine milking) and (2) simultaneously in six heifers at less than 100 d and in six heifers at greater than 200 d of gestation. Oxytocin responses to teat stimulation, including peak heights and area under the response curves, at 150, 200 and 250 d or at greater than 200 d of gestation were similar and were significantly greater than responses at 100 d or at less than 100 d. Responses to milking were lower at 90 d compared to responses at 30 d. Catecholamines were measured only during gestation and were generally not affected by teat stimulation. Epinephrine levels were significantly higher at 200 and 250 d compared to levels at 100 and 150 d. Baseline oxytocin concentrations and responses to teat stimulation were greatest at 150 d of gestation when epinephrine levels were still low, suggesting that stimulatory mechanisms responsible for the release of oxytocin develop and/or are expressed prior to the development of inhibitory sympathetic mechanisms. For norepinephrine, linear analyses did not show significant responses to teat stimulation overall. However, elevated norepinephrine responses (greater than .2 pmol/ml) following teat stimulation were seen in 28 of 51 trials, and large oxytocin responses (greater than 75 pg/ml/min) were seen predominantly only when norepinephrine responses were low (less than = .2 pmol/ml).
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PMID:Teat stimulation-induced oxytocin and catecholamine release in pregnant and lactating Holstein heifers. 207 May 99

Effects of oxytocin (OT) on the adrenal chromaffin tissue of male rats were examined by coupled morphometric and biochemical techniques. Synthetic OT was administered in doses of 0.14 and 0.25 IU/100 g/d during 7 or 10 consecutive days and the effects were followed 1, 24, 72 and 168 hours after the last injection. The function and structure of chromaffin cells were affected by the higher dose of OT only. They caused divergent responses on their amine contents. Adrenaline, noradrenaline and dopamine contents were increased, while serotonin content was decreased. These changes were different in duration and time of incidence. Stereological analysis showed an enhanced number of chromaffin cells and an increase in their total volume. The parallelism between the changes in chromaffin cell number and the catecholamine content strongly suggests a mitogenic effect of the applied OT.
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PMID:The response of rat adrenal medulla to oxytocin. 248 21

The substances stimulating the release of immunoreactive corticotropin-releasing factor from cultured human placental cells were investigated. Monolayer primary cultures of trophoblast cells from pregnant women at term were used. The immunoreactive corticotropin-releasing factor released in the culture medium eluted from high-performance liquid chromatography with the same retention time as human corticotropin-releasing factor. Norepinephrine and acetylcholine increased immunoreactive corticotropin-releasing factor release into the culture medium in a dose-related manner. Epinephrine was partially active, whereas dopamine and serotonin did not induce significant changes of immunoreactive corticotropin-releasing factor release from placental cultures. Angiotensin II, interleukin-1, oxytocin, and arginine-vasopressin also increased placental immunoreactive corticotropin-releasing factor release in a dose-related manner, whereas other peptides (vasoactive intestinal peptide, substance P, somatostatin, atrial natriuretic factor, interleukin-2) were ineffective. These results showed that several neurotransmitters and peptides stimulate the release of immunoreactive corticotropin-releasing factor from placental cells, suggesting their possible involvement in the physiologic regulation of placental immunoreactive corticotropin-releasing factor release during pregnancy and parturition.
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PMID:Neurotransmitters and peptides modulate the release of immunoreactive corticotropin-releasing factor from cultured human placental cells. 256 97


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