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)

Whole brain synaptosomes contain both an isorenin activity and angiotensin-related carboxypeptidase activity. Further hydrolysis of des-Leu angiotensin I (AI-dL) occurs more slowly; hydrolysis of angiotensin II (AII) is negligible. Vasopressin and oxytocin but not vasotocin can inhibit angiotensin-related carboxypeptidase activity. Since AII has been shown to induce vasopressin secretion, this correlation suggests a feedback inhibition by vasopressin of this enzymatic cascade. Commercially available radioimmunoassays for AI and AII show a 3.4 and 6.0% crossreactivity, respectively. When the absolute concentration of AI-dL exceeded 500 ng/ml, both antibodies to AI and AII showed maximal displacement of radiolabel. This suggests that these antibodies may not distinguish between AI-dL from other peptides during immunocytochemistry.
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PMID:Subcellular localization in rat brain of angiotensin-related carboxypeptidase activity distinct from converting enzyme. 319 54

Vasopressin (AVP) and oxytocin (OXT) were measured by radioimmunoassay in push-pull perfusates and tissue samples of various brain areas, plasma and cerebrospinal fluid (CSF) of male rats in response to osmotic stimulation. Hypertonic saline caused a significant rise in plasma AVP and OXT and different changes in peptide contents, in the septum and hippocampus at 30 and 60 min after intraperitoneal injection. Push-pull perfusion (20 microliters artificial CSF/min, 30-min periods) of the septum and dorsal hippocampus of conscious, unrestrained animals revealed a significant, stimulus-evoked release of both AVP and OXT. This release was: (1) not always reflected by corresponding changes in the regional peptide content; (2) simultaneous with the peripheral release from the posterior pituitary; and (3) probably the result of synaptic/parasynaptic events as suggested by use of agents in the artificial CSF which either inhibit or facilitate the release from intact fibre terminals.
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PMID:Central and peripheral release of vasopressin and oxytocin in the conscious rat after osmotic stimulation. 321 51

Vasopressin may act in the brain as a neurotransmitter or neuromodulator to influence blood pressure, memory, body temperature and brain development. In order to localize probable central nervous system sites for these actions, we have used 125I-labelled 1-d(CH2)5, 7-sarcosine-8-arginine vasopressin, a specific V1-receptor antagonist, and in vitro autoradiography to map brain vasopressin binding sites. High levels of binding were found in the choroid plexus, blood vessels, lateral septum, bed nucleus of stria terminalis, accumbens nucleus, central nucleus of amygdala, stigmoid hypothalamic nucleus, suprachiasmatic nucleus, arcuate nucleus, nucleus of the solitary tract, area postrema and parts of the hippocampus, thalamus, superior colliculus, and inferior olivary nuclei. Many of these regions are known to be vasopressin-sensitive and to contain vasopressin fibres. Significantly there was no binding to the paraventricular nor the supraoptic nuclei. Displacement of the radioligand from the lateral septum with unlabelled vasopressin analogues gave a rank order of potencies: d(CH2)5-D-Tyr2(Et)Val4-desGly9-arginine-vasopressin approximately equal to d(CH2)5-Tyr2-(Me)arginine-vasopressin approximately equal to arginine-vasopressin approximately equal to d(CH2)5-Sar7-arginine-vasopressin greater than [1-deamino, 8-D-arginine]-vasopressin approximately equal to oxytocin much greater than vasopressin4-9, consistent with binding to V1 receptor subtype. These studies confirm and extend previous findings of V1 receptors in the rat brain. In particular, several new regions of vasopressin receptor binding have been identified, possibly due to the advantages of a radioiodinated ligand with high receptor affinity without binding to neurophysins. Future study of these regions may prove fruitful in elucidating the central actions of vasopressin.
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PMID:Localization of vasopressin binding sites in rat brain by in vitro autoradiography using a radioiodinated V1 receptor antagonist. 325 72

The relative dependence or independence of the secretion of the neurohypophysial hormones, arginine vasopressin and oxytocin, was investigated using a wide variety of stimuli reported to cause the secretion of one or the other hormone. Differences in species, animal preparations, sampling techniques, assays, and other factors make comparison of many previous studies difficult. The aim of this study was to overcome these problems by using the same methodology, animal species, and assays to compare vasopressin and oxytocin release. To further strengthen the analysis, determinations of vasopressin and oxytocin were done in the same blood samples. The results demonstrated that during simultaneous release of both hormones, vasopressin is released in greater proportion following restraint stress, hemorrhage, isotonic hypovolemia, and nicotine, whereas oxytocin is released in greater proportion following endotoxin or hypertonic saline. Vasopressin was released without oxytocin following diethylstilbestrol. Oxytocin was released without concomitant vasopressin release following exercise, hypothermia, hyperthermia, labour, and lactation. Neither oxytocin nor vasopressin release was observed following thyroid-releasing hormone or insulin-induced hypoglycemia. These data illustrate the marked flexibility of the hypothalamo-neurohypophysial system that regulates secretion of vasopressin and oxytocin.
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PMID:Simultaneous and independent release of vasopressin and oxytocin in the rat. 337 May 33

Vasopressin (VP)-like immunoreactivity (IR) has been located in the testes of several species of mammal. There is evidence that most of this IR in the rat does not represent authentic arginine vasopressin (AVP) and that a second AVP-like peptide may exist. We have studied testis samples from the pig, which produces lysine vasopressin (LVP) in its pituitary, and have found both LVP- and AVP-like IR. High-performance liquid chromatography (HPLC) of testis extracts showed two peaks of VP-IR. The first peak co-eluted with authentic LVP and was recognized only by antisera which cross-reacted with LVP. The second peak co-eluted with authentic AVP and was recognized by antisera raised against AVP. Both VP-like peptides bound to a neurophysin affinity column and the HPLC elution profiles of the bound peptides were similar to those of the authentic hormones. When the LVP-like material was oxidized with performic acid, a peak of IR running in the same position as oxidized authentic LVP on HPLC was produced. Similarly, the performic acid-oxidized AVP-like material co-eluted with oxidized authentic AVP. The presence of both LVP- and AVP-like peptides in the pig testis may mean that more than one gene is involved. A second VP-like gene could also explain the anomalies of VP-IR in other species.
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PMID:Two vasopressin-like peptides in the pig testis? 339 99

Vasopressin-like immunoreactivity was detected in the auditory brainstem of female guinea pigs. Stained cell bodies and fibres were found in the inferior colliculus and in the ventral trapezoid body, and immunoreactive fibres in the dorsal cochlear nucleus. No vasopressin immunoreactivity was detected in the auditory brainstem of male guinea pigs. Using oxytocin antisera we found neither immunoreactive perikarya nor fibres in the auditory pathways of guinea pigs of both sexes.
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PMID:A sexually dimorphic vasopressin innervation of auditory pathways in the guinea pig brain. 342 75

Vasopressin and oxytocin exert pronounced effects on behaviour by a direct action on the brain. A single injection of vasopressin results in a long-term inhibition of extinction of a conditioned avoidance response suggesting that vasopressin triggers a long-term effect on the maintenance of a learned response, probably by facilitation of memory processes. In addition vasopressin improves passive avoidance behaviour, delays extinction of appetitive discrimination tasks, affects approach behaviour to an imprinting stimulus in ducklings, improves copulation rewarded behaviour of male rats in a T-maze, prevents or reverses amnesia induced by electroconvulsive shock, CO2 inhalation, pentylenetetrazol or puromycin. The majority of these effects of vasopressin in the various and sometimes relatively complex tasks may be explained by stimulatory influences of this neuropeptide on memory processes. Generally oxytocin exerts effects which are opposite to those of vasopressin and it has been suggested that oxytocin may be an amnesic neuropeptide. Various limbic system structures seem to act as the anatomical substrate for the behavioural effects of vasopressin. In particular the amygdala, the dentate gyrus of the hippocampal complex, the ventral hippocampus and the dorsal septum seem to be involved. Evidence has been obtained from experiments with homozygous diabetes insipidus rats and from experiments in which antisera were applied that endogenous vasopressin and oxytocin play a physiological role in brain processes related to memory. It appears that highly active fragments can be generated from vasopressin and experiments in which a fragment of vasopressin ([pGlu4, Cyt6]AVP-(4-8)) as well as an AVP-antagonist were used, reveal that the vasopressin receptors mediating the behavioural effects are situated in the brain and differ in specificity from the peripheral (blood pressure) vasopressin receptors. Generally the clinical data obtained so far with vasopressin treatment are in agreement with the results from animal experiments and they support the notion on the involvement of vasopressin in memory function. The sometimes reported conflicting results on vasopressin effects in certain patients (Korsakoff or Alzheimer) may have to do with the wide-spread pathology in these diseases.
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PMID:Vasopressin and oxytocin. Their presence in the central nervous system and their functional significance in brain processes related to behaviour and memory. 346 10

Since neuroimmunomodulation is brought about in part, at least, by secretion of pituitary hormones involved in stress and immune responses, we review briefly the hypothalamic control of the release of ACTH, growth hormone, and prolactin. The release of ACTH is controlled particularly by corticotropin-releasing factor (CRF), but vasopressin has intrinsic releasing activity and potentiates the action of CRF at both hypothalamic and pituitary levels. Oxytocin may even potentiate the action of CRF, but has little, if any, ACTH-releasing activity by itself. In addition, epinephrine may augment responses to the CRFs. In contrast, growth hormone is under dual control by growth-hormone-releasing factor (GRF) and somatostatin, and prolactin is under multifactorial control by a series of inhibitors and stimulators. Dopamine is accepted as a physiological prolactin-inhibiting factor (PIF), but probably GABA and possibly acetylcholine as well are PIFs. There is good evidence for a peptide PIF as well. There are a number of prolactin-releasing factors (PRFs) which include oxytocin, vasoactive intestinal polypeptide, PHI and TRH. Several other peptides can also release prolactin, including angiotensin II. In response to stress there is a complex interaction of peptides intrahypothalamically. CRF augments its own release by an ultra short-loop positive feedback, and there is negative ultra short-loop feedback of GRF and somatostatin. Vasopressin appears to augment CRF release as well as to act directly on the pituitary, and there are complex interactions of various peptides to influence prolactin and GH release.
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PMID:The role of brain peptides in neuroimmunomodulation. 347 67

The nature of the activity of vasopressin that is responsible for the inhibition of renin secretion was studied in normally hydrated conscious dogs using intravenous infusions of vasopressin and analogues of vasopressin with selective antidiuretic and vasoconstrictor activity. Vasopressin (1.0 ng . kg-1 . min-1) increased mean arterial pressure (MAP) from 106 +/- 2 to 115 +/- 3 mmHg (P less than 0.05) and decreased heart rate (HR) from 81 +/- 6 to 56 +/- 5 beats/min (P less than 0.001). Plasma renin activity (PRA) decreased from 4.4 +/- 1.1 to 2.4 +/- 0.8 ng . ml-1 . 3 h-1 (P less than 0.05). A specific antagonist of the vasoconstrictor activity of vasopressin, d(CH2)5MeTyrAVP (10 micrograms/kg), completely blocked the cardiovascular and renin responses to vasopressin. A selective vasoconstrictor agonist, 2-phenylalanine-8-ornithine oxytocin (1.0 ng . kg-1 . min-1), increased MAP from 112 +/- 4 to 128 +/- 6 mmHg (P less than 0.001) and decreased HR from 69 +/- 3 to 47 +/- 4 beats/min (P less than 0.001). PRA decreased from 5.5 +/- 1.1 to 2.7 +/- 0.2 ng . ml-1 X 3 h-1 (P less than 0.001). In contrast, a selective antidiuretic agonist, 1-deamino-8-D-arginine vasopressin (1.0 ng . kg-1 . min-1) did not alter PRA, MAP, or HR. These results demonstrate that the acute inhibition of renin secretion by vasopressin in normally hydrated conscious dogs is due to vasoconstrictor rather than antidiuretic activity.
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PMID:Role of the vasoconstrictor and antidiuretic activities of vasopressin in inhibition of renin secretion in conscious dogs. 351 May 66

Immunoperoxidase staining was applied to the hypothalamus and posterior pituitary of the camel. Vasopressin and oxytocin cells and fibers were identified in different nuclei of the hypothalamus. Immunoreactive fiber tracts were followed to the median eminence and the posterior pituitary. In the median eminence, two different pathways were found for vasopressin, one passing to the posterior lobe and the other contacting capillaries of the portal system. The oxytocin antiserum stained one unique pathway in the internal zone on its way to the posterior pituitary. The two immunoreactivities were shown in the posterior lobe of the pituitary, vasopressin staining being the more intense. Relations between these data and the physiology of the camel are discussed.
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PMID:Immunocytochemical evidence for vasopressin and oxytocin pathways in the hypothalamo-hypophyseal axis of the camel (Camelus dromedarius). 355 15


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