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)

Although neurohypophysial peptides are present in many regions of the developing and adult bullfrog (Rana catesbeiana) brain, the function of these peptides remains unclear. To investigate possible behavioral actions, we examined locomotor activity following peptide injection in bullfrogs at various developmental stages. An intraperitoneal (ip) injection of arginine vasotocin (AVT) in tadpoles (stages V, X, or XVII) produced an immediate and dose-dependent inhibition of locomotor activity. On the other hand, AVT stimulated activity when administered ip to juvenile or adult female bullfrogs, but did not influence activity in juvenile or adult males. The minimum effective dose of AVT, when injected directly into the brain of tadpoles, was 100-fold less than that observed when injected ip, suggesting a central nervous system site of action for this peptide. A vasopressin receptor antagonist (d(CH2)5[Tyr(Me)2]AVP administered ip or icv) significantly increased locomotor activity in tadpoles, compared to controls. Oxytocin, vasopressin, and AVP4-9 inhibited activity in tadpoles while mesotocin, des Gly(NH2)AVP, and pressinoic acid had no significant effect. Injection of PGF2 alpha also significantly decreased activity levels in tadpoles. However, pretreatment of tadpoles with indomethacin, a prostaglandin synthesis inhibitor, did not prevent the behavioral effects of AVT, suggesting that prostaglandin synthesis is not required for this response. In summary, AVT influenced locomotor activity in bullfrog tadpoles and female frogs. This effect shifted during development from an inhibitory action in tadpoles to a stimulatory effect in metamorphosed female frogs. The effect of AVT on juvenile and adult frog locomotion was sexually dimorphic, as this peptide altered female behavior but not male behavior.
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PMID:Effect of vasotocin on locomotor activity in bullfrogs varies with developmental stage and sex. 204 91

The neurotransmitter histamine participates in the neuroendocrine regulation of pituitary hormone secretion by an indirect action at a hypothalamic level where histaminergic neurons are abundant. The effect of histamine is caused by activation of postsynaptic H1- or H2-receptors. Histamine stimulates the secretion of ACTH, beta-endorphin (mediated by CRH and AVP), alpha-MSH (mediated by dopamine and peripheral catecholamines), and PRL (mediated by dopamine, serotonin and AVP), and participates in the stress-induced release of these hormones and possibly in the suckling- and estrogen-induced PRL release. The release of GH and TSH is predominantly inhibited by histamine; however, uncertainty exists regarding its role and the hypothalamic factors involved. Histamine increases the secretion of LH in females (mediated by GnRH), and may be involved in the mediation of the estrogen-induced LH surge. AVP and oxytocin are stimulated by histamine, probably by an effect in the supraoptic and paraventricular nuclei of the hypothalamus.
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PMID:The role of histamine in the neuroendocrine regulation of pituitary hormone secretion. 206 91

Recent results have demonstrated altered corticotropin-releasing factor (CRF)-41 content of the neurointermediate lobe (NIL) of the pituitary gland in response to various manipulations including osmotic stimulation. This study was undertaken to determine whether changes in CRF-41 content of the NIL are accompanied by changes in intensity of CRF-41-like immunoreactivity (CRF-41-LI) of neurosecretory neurones of the hypothalamus in response to osmotic stimulation. Wistar rats of both sexes given either tap water ad libitum, 2% NaCl solution, or access to tap water was limited to 20 min daily, for 7 days. Subsets of rats from each group were adrenalectomized (ADX) or treated with dexamethasone (DEX). Thirty-six hour before perfusion with fixative consisting of buffered formaldehyde and picric acid, animals received 75 micrograms colchicine i.c.v. Forty micrometer thick vibratome sections were stained for CRF-LI, arginine vasopressin (AVP-LI) and oxytocin (OXY-LI) using the avidin-biotin-peroxidase complex method. In response to both types of osmotic stimulation magnocellular neurones of the paraventricular (PVN) and supraoptic nuclei (SON) showed increased CRF-LI, AVP-LI and OXY-LI, while CRF-LI of parvocellular perikarya of the PVN decreased. The enhanced CRF-LI seemed to appear in a subset of magnocellular neurones with OXY-LI but not AVP-LI. Increased staining intensities were also observed in magnocellular neurones in ADX rats challenged osmotically. In contrast, systemic DEX administration, as well as implantation of DEX in the area on the SON, sharply attenuated CRF-LI but not AVP-LI or OXY-LI of magnocellular neurones in osmotically stimulated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxytocinergic neurons in rat hypothalamus. Dexamethasone-reversible increase in their corticotropin-releasing factor-41-like immunoreactivity in response to osmotic stimulation. 211 29

1. Intracerebroventricular (I.C.V.) injections of isotonic and hypertonic solutions into the dorsal (D3V) and ventral (V3V) third ventricle were employed to examine the release of vasopressin (AVP) and the mean arterial pressure (MAP) response to elevated cerebrospinal fluid (CSF) osmolality in the conscious rat. 2. The D3V injection of hypertonic sodium chloride solution was associated with a concentration-dependent, transient increase in plasma AVP concentration and MAP. 3. The D3V injection of 5 microliters 0.85 M-sodium chloride elicited a 7-fold increase in plasma AVP and oxytocin concentrations, but had no effect on plasma ACTH concentration. The D3V injection of 1.11 M-mannitol in 0.15 M-sodium chloride had no effect on plasma AVP concentration or MAP. However, the D3V injection of 0.746 M-mannitol in 0.4 M-sodium chloride elicited a significant transient increase in plasma AVP, but had no effect on MAP. 4. The V3V injection of 5 microliters 0.85 M-sodium chloride elicited a prolonged increase in plasma AVP concentration and a transient increase in MAP. The V3V injection of 5 microliters 1.11 M-mannitol in 0.15 M-sodium chloride elicited an equal, but transient, increase in plasma AVP concentration, but had no effect on MAP. 5. The pressor effect of a D3V injection of 0.85 M-sodium chloride was unaffected by prior administration of the V1 (pressor) receptor antagonist (beta-mercapto-beta,beta-cyclopentamethylene propionyl1, O-Me-Tyr2, Arg8)-vasopressin. 6. These results indicate that osmotically induced AVP secretion may be mediated by both sodium receptors and osmoreceptors, although expression of the response may depend upon the maintenance of a 'permissive' concentration of sodium in the CSF. 7. It appears also that the pressor effect is not due to increased plasma AVP concentration, but only results from elevation of the CSF sodium concentration.
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PMID:The vasopressin response to centrally administered hypertonic solutions in the conscious rat. 212 Apr 29

Immunochemical studies associated with physicochemical procedures led to demonstrate the presence of neurohypophysial-like peptides in the testis of numerous species including human. Characterization of arginine-vasopressin-neurophysin II mRNA and oxytocin-neurophysin I mRNA in rat testicular extracts is in favour of a local production for these peptides. The in vitro and in vivo evidences of a direct regulation of testicular steroidogenesis bg AVP and related peptides--the identification of specific AVP receptors on purified Leydig cells and their alteration in some physiological or pathological situations argue for a paracrine/autocrine role of these neurohypophysial-like-peptides in modulating Leydig cell androgen biosynthesis.
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PMID:[Intragonadal control of testicular function by neurohypophyseal-like peptides]. 213 Jul 61

Arginine (AVP) and lysine vasopressin induce a weak but statistically significant increase in the water permeability of Amoeba proteus plasmalemma. Vasotocin and deaminovasopressin, which share the hydroosmotic properties of AVP on classical vertebrate systems, are without effects on Amoeba while SKF 101926, a synthetic AVP antagonist, is even more effective than the parent compound. Theophyllin and dibutyryl-cAMP do not affect AVP action on Amoeba. Lithium, oxytocin, and carbachol are also without effect. Thus, it is unlikely that either V2 (cAMP) or V1 (phosphatidylinositol choline) receptors are involved. A clear correlation has been found between the amphiphilic character of tested peptides and their effect on Amoeba water permeability. Classical amphiphilic peptides, melittin, mastoparan, and fragment 1-8 of alpha-neoendorphin, also increased water permeability in Amoeba. It is known that vasopressin can interact with artificial lipid membranes, increasing their permeability to water. We propose that amphiphilic members of the AVP family interact directly with the lipid phase of the Amoeba membrane. Their incorporation within the lipid bilayer may cause local disruptions or may create micellar water channels as shown for other amphiphilic proteins. Our observations provide a model for the early evolution of peptide hormone systems, preceding the appearance of specific membrane receptors and associated second messenger amplifying mechanisms.
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PMID:The amphiphilic action of vasopressin and analogues on the plasma membrane of Amoeba proteus. 214 31

Arginine vasopressin is a neuropeptide that has been shown to modulate functional ethanol tolerance and memory processes. These actions of vasopressin in the CNS have been shown by us and others to be mediated by V1 receptors. Intracerebroventricular injection of vasopressin in mice resulted in a substantial increase in mRNA for the proto-oncogene c-fos in septum and hippocampus, but no increase in cerebral cortex. A V1-selective agonist also increased septal c-fos mRNA levels, while a V2-selective agonist was less effective. Similarly, the response to vasopressin was more effectively blocked by a V1- than a V2-selective antagonist. These results indicate that vasopressin acts specifically at V1 receptors in mouse septum and hippocampus to increase c-fos mRNA. The vasopressin metabolite, AVP(4-9), also increased c-fos mRNA levels in septum and hippocampus, while the response to oxytocin, which has different effects from vasopressin on memory and tolerance, was greater in hippocampus than in septum. Nerve growth factor, in contrast to the other peptides, had a more pronounced effect on c-fos mRNA levels in cerebral cortex than in the other brain areas. Increased c-fos expression has been hypothesized to play a role in neuroadaptation, and these results suggest that modulation of septal c-fos expression could be important for vasopressin effects on ethanol tolerance and/or memory.
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PMID:Arginine vasopressin induces the expression of c-fos in the mouse septum and hippocampus. 216 40

The binding of 3H-oxytocin (3H-OT) and 3H-arginine-vasopressin (3H-AVP) and the displacement from binding sites by four oxytocin analogues were studied in myometrial membrane preparations from full-term pregnant women. Specific 3H-OT binding was saturable with a maximal binding capacity of 76.1 fmol/mg DNA, and a dissociation constant of 0.5 pM. Corresponding values regarding 3H-AVP was 148.6 fmol/mg DNA and 0.7 pM. The oxytocin analogues tested demonstrated a high specific binding to the OT and AVP receptor sites; in fact, the affinity of the analogues to the 3H-AVP binding sites was higher than to the 3H-OT binding sites. The order of potency between the analogues was CAU greater than CAM greater than CAP greater than CAO and CAP greater than CAU greater than CAO greater than CAM for the OT and AVP binding sites, respectively. The displacement of oxytocin and arginine-vasopressin, respectively, from the myometrial receptor sites indicate partly separate binding sites for oxytocin and AVP and might implicate that AVP can be of importance in regulating myometrial activity in pregnancy. The results on oxytocin analogues imply that other pharmacological tests must be performed for quantification of the relaxing effects on the uterus and to determine the optimal analogue for clinical trials in preterm labor and dysmenorrhoea.
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PMID:Binding of four oxytocin analogues to myometrial oxytocin and arginine-vasopressin binding sites in pregnant women. 216 84

The binding of [3H]oxytocin ([3H]-OT) and [3H]arginine vasopressin ([ 3H]-AVP) by bovine endometrial and myometrial membrane preparations obtained on days 0, 7, 14, 17, and 21 after estrus or mating was investigated. [3H]OT was bound with higher affinity than [3H]AVP by both tissues; the mean dissociation constants (KdS) were 0.95 x 10(-9) M and 1.56 x 10(-9) M for OT and AVP, respectively, P less than 0.0001, with no significant variations in the KdS during the cycle. The concentration of [3H]OT binding sites was on the average 50% higher than [3H]AVP across the cycle in both tissues. Endometrial receptor levels varied significantly during the cycle; it was lowest on days 7 and 14, rose significantly on day 17, and peaked on day 21. Myometrial receptor levels decreased from levels at estrus on days 7 and 14, but the changes were not significant. The ratio between endometrial and myometrial receptor concentrations changed from about 10 at estrus to less than 1 in the luteal phase. In early pregnancy, the receptor levels did not differ from nonpregnant levels on days 7 and 14, but on day 17 the endometrial receptor concentrations were significantly lower, and on day 21 those in both tissues were significantly lower. The endometrial OT and AVP receptor concentrations were inversely correlated with plasma progesterone levels (P = 0.005) with no correlation to plasma estradiol, whereas the myometrial receptor concentrations showed no correlation to plasma progesterone but an inverse correlation with plasma estradiol (P = 0.004). We conclude that the endometrial OT and AVP receptor concentrations are more tightly controlled by progesterone than myometrium, and that the bovine conceptus suppresses endometrial OT and AVP receptor concentrations in the preattachment stage either by a local action on the endometrium or indirectly via an antiluteolytic effect.
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PMID:Oxytocin and vasopressin receptors in bovine endometrium and myometrium during the estrous cycle and early pregnancy. 216 15

In animals, there is sexual dimorphism of both neurohypophysial peptide secretion in response to stressful stimuli and to the inhibitory effects of opioids. In men, endogenous opioids inhibit the release of oxytocin when AVP secretion is stimulated by insulin-induced hypoglycemia. We have now investigated the role of endogenous opioids in the AVP and oxytocin response to insulin-induced hypoglycemia in women. Twelve subjects, 6 in the follicular and 6 in the luteal phase of the menstrual cycle, were infused on 2 occasions with naloxone (4 mg bolus and 6 mg/h) or saline. Soluble insulin (Human Actrapid, 0.15 mu/kg, iv) was given and serial blood samples taken. Blood sugar fell significantly (p less than 0.05) and similarly in all groups. In the follicular phase hypoglycemia led to a rise in plasma AVP from 1.3 +/- 0.2 to 1.8 +/- 0.2 pmol/l in the saline-infused subjects (NS), and from 1.0 +/- 0.1 to 2.0 +/- 0.2 pmol/l in the naloxone-infused (p less than 0.05). AVP rose similarly from 0.6 +/- 0.1 to 1.6 +/- 0.5 pmol/l (p less than 0.05) in the luteal phase controls and from 0.8 +/- 0.1 to 1.5 +/- 0.3 pmol/l (p less than 0.05) in naloxone-infused subjects in the luteal phase. There were no significant differences between any of these groups. There were no significant changes in plasma oxytocin in any group. We therefore conclude that in women, unlike men, endogenous opioids do not modulate oxytocin or vasopressin release during insulin-induced hypoglycemia.
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PMID:Neurohypophysial secretion to insulin-induced hypoglycemia and its regulation by endogenous opioids in women. 218 2


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