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

Noradrenaline stimulates the concomitant release of ovarian oxytocin and progesterone in cattle within a few minutes, but the mechanism of its action is unknown. Changes in alpha- and beta-receptors and blood pressure were considered as possible mechanisms of the noradrenaline effect. Heifers in group 1 (n = 4) were infused with noradrenaline (0.16 microgram kg-1 min-1) for 30 min into the aorta abdominalis (cranial to the origin of the ovarian artery) on day 10. On days 11 and 12 before noradrenaline, phentolamine (alpha-blocker; 30 micrograms kg-1 min-1) or propranolol (beta-blocker; 5 micrograms kg-1 min-1) were infused for 30 min. Four other heifers were infused with noradrenaline only as controls. Only propranolol inhibited the stimulatory effect of noradrenaline on the secretion of progesterone and oxytocin. In group 2, heifers (n = 4) were infused, making use of the latin square design, with vasoconstrictive (angiotensin; 0.042 microgram kg-1 min-1) or vasodilatory (xanthinol-theophylline nicotinate; 250 micrograms kg-1 min-1) drugs that do not act through the adrenoceptors. Noradrenaline (0.3 microgram kg-1 min-1) was given 1 h later as in group 1. Blood pressure changes were measured in the posterior aorta abdominalis and oxytocin and progesterone concentrations were determined in the blood samples collected from the jugular vein. Noradrenaline and angiotensin increased (P < 0.01), whereas xanthinol decreased (P < 0.01), blood pressure during their infusion. However, the rise of oxytocin and progesterone concentrations was observed only after noradrenaline infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of noradrenaline influence on the secretion of ovarian oxytocin and progesterone in conscious cattle. 838 56

Mature heifers (n = 31) were infused with either saline or noradrenaline (0.3 microgram kg-1 min-1) via a cannula inserted into the aorta abdominalis through the coccygeal artery (cranial to the origin of the ovarian artery). Noradrenaline was infused for three periods of 30 min on days 11 and 12 and on days 15 and 16 of the oestrous cycle. After the noradrenaline treatment, saline was given for 1 h in the same way. During each infusion, peripheral blood samples were collected for progesterone and oxytocin determination every 5-10 min and then once a day until oestrus. As a control, four heifers were infused with saline in latin square design on days 11, 12 and on days 15, 16; they were bled once a day until oestrus. Other heifers were infused on the same days, but 1 h after the last infusion of noradrenaline, 500 micrograms of prostaglandin F2 alpha (PGF2 alpha) analogue was injected, to measure any remaining luteal oxytocin. For comparison four heifers were injected with PGF2 alpha analogue alone on day 12 and four others on day 16. Blood samples were taken as described previously. Each infusion of noradrenaline stimulated (P < 0.01) progesterone secretion. There was a significant (P < 0.05) response of oxytocin to each noradrenaline stimulation on days 11 and 12, although on each day the response to the second infusion was reduced and further reduced after the third infusion. On days 15 and 16, only the first noradrenaline infusion caused a clear surge of oxytocin with much smaller increases in oxytocin secretion after subsequent infusions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of oxytocin removal from the corpus luteum on secretory function and duration of the oestrous cycle in cattle. 850 12

Oxytocin (OT) release within the brain is thought to play a major role in inducing maternal behaviour in a number of mammalian species but little is known about the sites of release which are important in this respect. We have investigated whether the paraventricular nucleus of the hypothalamus (PVN) is a site of OT action on maternal behaviour in the sheep. In vivo microdialysis and retrodialysis was used to determine whether OT is released in the region of the PVN during the post-partum induction of maternal behaviour and if its release at this site can stimulate maternal behaviour in non-pregnant animals. In vivo sampling showed that OT concentrations increased significantly in the region of PVN at birth. When OT was retrodialysed bilaterally into the PVN (1 or 10 microM) of multiparous ewes treated with progesterone and oestradiol to stimulate lactation, maternal behaviour was induced in a significant number of animals (1 microM, 6/8 and 10 microM, 5/8) compared with controls (0/8 ewes). Similar infusions of the ring structure of OT, tocinoic acid (TOC-10 microM), also induced maternal behaviour in a significant proportion of animals (5/6 ewes) as did intracerebroventricular (ICV) OT (6/8 ewes) and artificial stimulation of the vagina and cervix (VCS, 8/9 ewes). On the other hand, vasopressin (AVP) 1 microM did not induce maternal behaviour in any ewes and a 10 microM dose only induced it in 2/8 animals. The neurochemical changes accompanying the above treatments were also investigated. Noradrenaline concentrations increased in the PVN after the retrodialysis administration of OT 1 microM and 10 microM, TOC 10 microM and AVP 1 microM, OT ICV and VCS. Dopamine concentrations were also increased by OT 10 microM, TOC 10 microM, AVP 1microM and OT ICV. Aspartate and glutamate concentrations were significantly reduced by retrodialysis infusions of OT 1 microM and AVP 1 and 10 microM but not by any other treatment. Finally, the retrodialysis infusion of OT and TOC, as well as ICV OT, significantly increased plasma OT release whereas AVP infusions did not. These results provide evidence that OT is released in the PVN during parturition and is important for the induction of maternal behaviour. It seems probable that OT release at this site has a positive feedback effect on both parvocellular and magnocellular OT neurons to facilitate co-ordinated OT release both in central OT terminal regions (to facilitate maternal behaviour) and peripherally into the blood (to facilitate uterine contractions/milk let down). The potential functional roles for the actions of OT on monoamine and amino acid transmitter release in the PVN are discussed.
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PMID:The role of oxytocin release in the paraventricular nucleus in the control of maternal behaviour in the sheep. 873 Jun 50

The peripheral pharmacology of local mechanisms of penile erection is known today thanks to recent advance in the study of the regulation of erectile tissue smooth muscle tone. Smooth muscle fibers present in the corpus cavernosum and arteries destined to the penis relax in response to the release of non adrenergic non cholinergic neuromediators synthetized by postganglionic parasympathetic nerve fibers present in the cavernous nerves. Nitric oxide is the main proerectile neuromediator. Noradrenaline, released by sympathetic fibers, contracts penile smooth muscle fibers and is antierectile. Recent progress in the peripheral pharmacology of penile erection allows new perspectives in the treatment of erectile dysfunction. The spinal cord represents a major site for the neural regulation of penile erection. The latter occurs in response to stimuli from peripheral or supraspinal origin. Different neural structures in the brainstem (nucleus paragigantocellularis), pons and hypothalamus (nucleus paraventricularis) send projections to the thoracolumbar sympathetic and lumbosacral parasympathetic nuclei at the origin of proerectile peripheral pathways. Serotonin and oxytocin are candidates as neuromediators involved in the supraspinal control of penile erection. Studying the central command of penile erection allows an approach to the pathophysiology of psychogenic erectile dysfunction.
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PMID:[Physiology of erection]. 918 54

Noradrenergic projections to the hypothalamus play a critical role in the afferent control of oxytocin and vasopressin release. Recent evidence for intrahypothalamic glutamatergic circuits prompted us to test the hypothesis that the excitatory effect of noradrenergic inputs on oxytocin and vasopressin release is mediated in part by local glutamatergic interneurons. The voltage response to norepinephrine (30-300 microM) was tested with whole-cell recordings in putative magnocellular neurons of the paraventricular nucleus (PVN) in hypothalamic slices (400 micrometers). Norepinephrine elicited an alpha1 receptor-mediated direct depolarization in 23% of the magnocellular neurons tested; however, the most prominent response, seen in 42% of the magnocellular neurons, was an alpha1 receptor-mediated increase in the frequency of EPSPs. The norepinephrine-induced increase in EPSPs was blocked by tetrodotoxin and by ionotropic glutamate receptor antagonists, suggesting that norepinephrine excited presynaptic glutamate neurons to cause an increase in spike-mediated transmitter release. The increase in EPSPs also was observed in a surgically isolated PVN preparation (64% of cells) and with microdrop applications of norepinephrine (1 mM, 33% of cells) and glutamate (0.5-1 mM, 28%) in the PVN, indicating that the norepinephrine-sensitive presynaptic glutamate neurons are located within the PVN. Biocytin injection and subsequent immunohistochemical labeling revealed that both oxytocin and vasopressin neurons responded to norepinephrine. Our data indicate that magnocellular neurons of the PVN receive excitatory inputs from intranuclear glutamatergic neurons that express alpha1-adrenoreceptors. These glutamatergic interneurons may serve as an excitatory relay in the afferent noradrenergic control of oxytocin and vasopressin release under certain physiological conditions.
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PMID:Noradrenergic excitation of magnocellular neurons in the rat hypothalamic paraventricular nucleus via intranuclear glutamatergic circuits. 985 97

Mammary deiodinase type I (M-D1) is present only during lactation and exhibits a clear direct correlation with lactation intensity (size of litters). The present work shows that M-D1 is suckling dependent and that intervals between suckling periods no longer than 12 h are essential to maintain this activity. Moreover, we find that with only 15 min of resuckling in 12-h nonsuckled mothers, the 50% decrease in both M-D1 messenger RNA and enzymatic activity could be restored to control values. This restorative effect by suckling may involve pre- and posttranscriptional mechanisms in which norepinephrine and PRL play important roles. Norepinephrine elicits a potent stimulatory effect on M-D1 messenger RNA and enzyme activities, whereas PRL only increases M-D 1 activity and may modulate the enzyme response to norepinephrine. Oxytocin and GH had no effect. These data suggest that the adrenergic nervous system and PRL could directly participate in mammary energetic expenditure, regulating the local T3 supply.
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PMID:Mammary type I deiodinase is dependent on the suckling stimulus: differential role of norepinephrine and prolactin. 1038 85

The localization and pharmacological characteristics of vasopressin (VP) binding sites of the V(1a) subtype in developing and adult rat kidney were investigated by radioautography on kidney sections incubated in the presence of a radioiodinated selective V(1a) antagonist. Their localization after in vivo systemic infusion of the radioligand was also investigated. V(1a) binding sites first appear at embryonic day 16 on vascular elements. In the adult, they were localized in the cortex (vascular and tubular structures, juxtaglomerular apparatus), the outer medulla outer stripe (vasa recta) and inner stripe (thin descending limbs of short looped nephrons) and the inner medulla (collecting ducts). Data obtained in vitro were confirmed by in vivo binding at postnatal day 30 (PN30). Whatever their localizations, the V(1a) binding sites exhibited full V(1a) pharmacological profile in postnatal stages rats and in adult rats: a high affinity (nM range) for VP and for the V(1a) agonist, a lower affinity (microM range) for oxytocin and no affinity for the oxytocin agonist. The presence of V(1a) binding sites in these different structures raises the question of the putative roles of VP in modulating renal functions. A striking finding is the presence of V(1a) binding sites in the outer medullary thin descending limbs of short looped nephrons suggesting their colocalization with urea transporters.
Nephron 1999 Sep
PMID:Historadioautographic localization, pharmacology and ontogeny of V(1a) vasopressin binding sites in the rat kidney. 1046 Oct 39

Noradrenergic projections to the hypothalamic paraventricular nucleus have been implicated in the secretory regulation of several anterior pituitary hormones, including adrenocorticotropin, thyroid-stimulating hormone, growth hormone and prolactin. In an attempt to elucidate the effects of norepinephrine on the central control of pituitary hormone secretion, we looked at the actions of norepinephrine on the electrical properties of putative parvocellular neurons of the paraventricular nucleus using whole-cell current-clamp recordings in hypothalamic slices. About half (51%) of the putative parvocellular neurons recorded responded to norepinephrine with either a synaptic excitation or a direct inhibition. Norepinephrine (30-300microM) caused a marked increase in the frequency of excitatory postsynaptic potentials in about 36% of the parvocellular neurons recorded. The increase in excitatory postsynaptic potentials was blocked by prazosin (10microM), but not by propranolol (10microM) or timolol (20microM), indicating that it was mediated by alpha(1)-adrenoreceptor activation. It was also blocked by ionotropic glutamate receptor antagonists, suggesting that the excitatory postsynaptic potentials were caused by glutamate release. The increase in excitatory postsynaptic potentials was completely abolished by tetrodotoxin, indicating the spike dependence of the norepinephrine-induced glutamate release. In a separate group comprising 14% of the parvocellular neurons recorded, norepinephrine elicited a hyperpolarization (6.2+/-0.69mV) that was blocked by the beta-adrenoreceptor antagonists, propranolol (10microM) and timolol (20microM), but not by the alpha(1)-receptor antagonist, prazosin (10microM). This response was not blocked by tetrodotoxin (1.5-3microM), suggesting that it was caused by a direct postsynaptic action of norepinephrine. The topographic distribution within the paraventricular nucleus of the norepinephrine-responsive and non-responsive parvocellular neurons was mapped based on intracellular biocytin labeling and neurophysin immunohistochemistry. These data indicate that one parvocellular subpopulation, consisting of about 36% of the paraventricular parvocellular neurons, receives an excitatory input from norepinephrine-sensitive local glutamatergic interneurons, while a second, separate subpopulation, representing about 14% of the parvocellular neurons in the paraventricular nucleus, responds directly to norepinephrine with a beta-adrenoreceptor-mediated inhibition. This suggests that excitatory inputs to parvocellular neurons of the paraventricular nucleus are mediated mainly by an intrahypothalamic glutamatergic relay, and that only a relatively small subset of paraventricular parvocellular neurons receives direct noradrenergic inputs, which are primarily inhibitory.
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PMID:Noradrenergic regulation of parvocellular neurons in the rat hypothalamic paraventricular nucleus. 1072 92

Noradrenaline (NA) influences secretory function of the bovine corpus luteum (CL), stimulating secretion of progesterone and ovarian oxytocin (OT). To study whether NA is able to stimulate progesterone synthesis and to affect post-translational OT processing, different doses of NA alone or in combination with different doses of OT were added to bovine CL slices from 8 to 13 d of the estrous cycle. To determine which receptors NA affects, and if dopamine (DA) also affects CL function, we used NA or DA combined with a beta-antagonist (propranolol). The results indicated that NA stimulates both luteal progesterone and OT content; furthermore, it increased the activity of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) and peptidyl glycine-alpha-amidating mono-oxygenase (PGA), terminal enzymes in synthesis of these 2 hormones. The stimulating effect of NA was inhibited by propranolol and by pre-treatment of CL slices with high OT doses. Post-translational processing of OT synthesis by PGA activation was also stimulated by DA, but this effect was inhibited by beta-receptor blocker. Thus DA acts in CL as a NA precursor. In conclusion, it can be assumed that the noradrenergic system affects CL secretory function on different levels of regulation. Furthermore, a high concentration of OT in CL prevents NA from activating PGA and thus decreases post-translational OT synthesis.
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PMID:Influence of noradrenaline on progesterone synthesis and post-translational processing of oxytocin synthesis in the bovine corpus luteum. 1073 8

The release of vasopressin and oxytocin is regulated by the electrical activity of magnocellular neurosecretory cells in the supraoptic and paraventricular nuclei, which is under the control of a great variety of neurotransmitters and neuromodulators. The major neural signals to the supraoptic nucleus are from excitatory glutamate inputs and inhibitory GABA inputs. In recent studies, the voltage-clamp mode of the whole-cell patch-clamp technique has been applied to slice preparations from rat hypothalamus to monitor synaptic inputs to supraoptic neurones. Spontaneous excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) are abolished by CNQX and picrotoxin, respectively, but are insensitive to tetrodotoxin, indicating that they represent quantal release of glutamate and GABA, respectively, from nerve terminals of presynaptic neurones. GABA and glutamate show remarkable suppressive effects on both EPSCs and IPSCs via presynaptic GABA(B) and mGlu receptors, respectively. Noradrenaline, which excites supraoptic neurones via postsynaptic alpha1-receptors, also suppresses IPSCs and potentiates EPSCs. On the other hand, prostaglandin E2, which excites supraoptic neurones via postsynaptic prostaglandin E2 (EP) receptors of the EP4 subclass, also suppresses IPSCs via EP3 receptors but has little effect on EPSCs. Thus pre- and postsynaptic mechanisms may act cooperatively to excite supraoptic neurones. Nitric oxide, which inhibits supraoptic neurones, potentiates IPSCs without affecting EPSCs. This provides another example for the preferential modulation of IPSCs of supraoptic neurones. On the other hand, PACAP, which causes a long-lasting increase in the firing frequency via the postsynaptic receptors, has no effect on EPSCs and IPSCs, suggesting that some ligands act only at postsynaptic receptors. Thus multiple patterns for pre- and postsynaptic modulation are present in the supraoptic nucleus, and the electrical activity of supraoptic neurones is regulated via complex mechanisms at both pre- and postsynaptic sites.
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PMID:Pre- and postsynaptic modulation of the electrical activity of rat supraoptic neurones. 1079 17


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