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)

A single class of high affinity, low capacity, specific binding sites for [3H]arginine8 vasopressin (AVP) has been characterized in a plasma membrane-enriched microsomal fraction of the rat liver. Specific binding was saturable, linear with protein concentration, reversible, and 40-65% of the total binding. Binding at 25 C achieved a plateau after 30 min of incubation, whereas at 4 C, equilibrium was reached more slowly, and the level of binding was reduced. The presence of magnesium (Mg2+) in the assay medium enhanced the affinity of specific binding, while calcium and higher levels of sodium and potassium decreased binding. Scatchard analysis of binding in the presence of Mg2+ (5 mM) revealed an apparent mean +/- SE equilibrium dissociation constant (Kd) of 0.29 +/- 0.08 nM, with a maximal site density (Bmax) of 150.4 +/- 25.0 fmol/mg; in contrast, the Kd was 1.93 +/- 0.33 nM and the Bmax was 113.4 +/- 40.0 fmol/mg in the absence of Mg2+. No significant differences in Kd and Bmax were observed among membrane fractions derived from spontaneously hypertensive rats, Wistar-Kyoto rats, Long-Evans rats, and Brattleboro rats. Plasma levels of AVP were similar in spontaneously hypertensive, Wistar-Kyoto, and Long-Evans rats, but AVP was not detectable in the plasma from DI rats. Competitive inhibition of specific [3H]AVP binding by unlabeled AVP and related peptides showed the following Ki values: AVP, 0.19 nM; LVP, 1.7 nM; oxytocin, 41.4 nM; desamino AVP, 0.38 nM; [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid) 4-Val,8-D-Arg] VP2-(O-methyl)tyrosine]AVP, 1.8 nM; desglycinamide AVP, 2.2 microM. The neuropeptide metabolite of AVP [[pGlu4,Cyt6] AVP-(4-9)], angiotensin II, and other unrelated peptides did not displace [3H]AVP, demonstrating the specificity of AVP and its related biologically active peptides for this binding site. Moreover, the rank order of potency for displacement of [3H]AVP binding by these various peptides parallels their reported glycogenolytic activity in liver and/or their agonistic or antagonistic potency in vascular smooth muscle. Finally, the Mg2+-induced increase in the affinity of [3H]AVP for this liver binding site is similar to the reported effect of Mg2+ on the contractile responses of vascular smooth muscle to AVP (i.e. increased affinity). The results are consistent with the interpretation that the high affinity receptor site characterized in rat liver microsomes is of the V1 type.
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PMID:Characterization of a specific, high affinity [3H]arginine8 vasopressin-binding site on liver microsomes from different strains of rat and the role of magnesium. 300 5

The angiotensin II (AII) sensitivity of neurons in the supraoptic nucleus (SON), subfornical organ (SFO) and the region near the anteroventral part of the third ventricle (AV3V) was investigated using extracellular recording in the rat brain slice preparation by adding AII (10(-10)-10(-6) M) to the perfusion medium. Forty seven (44%) of 106 SON neurons, 62 (66%) of 94 SFO neurons and 28 (33%) of 86 AV3V neurons were excited by AII. One cell was inhibited by AII in the SON and one in the SFO. The threshold concentration to evoke responses in the SON neurons was approximately 10(-9) M, but neurons in the SFO and AV3V showed clear excitatory responses to AII at 10(-10) M. In the SON, 18 (40%) of 45 phasic firing neurons (putative vasopressin neurons) and 29 (48%) of 61 nonphasic firing neurons (including putative oxytocin neurons) were excited by AII. The excitatory effect of AII was reversibly antagonized by a specific antagonist saralasin and persisted after synaptic blockade in medium with low [Ca2+] and high [Mg2+]. We conclude that AII can stimulate both vasopressin and oxytocin release, acting directly upon SON neurons and also that both the SFO and AV3V are important receptive sites for AII (although the SFO is relatively more sensitive) which contributes SON input and modulates release of these hormones.
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PMID:Angiotensin II sensitive neurons in the supraoptic nucleus, subfornical organ and anteroventral third ventricle of rats in vitro. 303 Apr 93

Carp (Cyprinus carpio) liver maintained normal glycogen content and enzyme complement for several days in organ culture. Epinephrine-stimulated glycogenolysis, phosphorylase activation, and cyclic AMP (cAMP) accumulation in a concentration-dependent manner with EC50s of 100, 100, and 500 nM, respectively. These actions were blocked by the beta-adrenergic antagonist, propranolol, but not by the alpha-adrenergic antagonist phentolamine. Glycogenolysis and tissue cAMP were uninfluenced by 10(-6) M arginine vasotocin, arginine vasopressin, lysine vasotocin, lysine vasopressin, mesotocin, or oxytocin, but were slightly increased by 10(-5) M isotocin and slightly decreased by 10(-6) M angiotensin II. [125I]-iodocyanopindolol (ICP), a beta-adrenergic ligand, bound to isolated carp liver membranes with a KD of 83 pM. Maximum binding of 45 fmol/mg protein was at 600 pM. Propranolol, isoprenaline, epinephrine, phenylephrine, norepinephrine, and phenoxybenzamine displaced ICP with KDs of 100 nM, 2, 20, 20, 60, and 200 microM, respectively. The alpha-adrenergic antagonists, yohimbine and prazosin, showed no specific binding. These data provide evidence that catecholamines act via beta-adrenergic receptors in carp liver and that alpha-adrenergic receptors are not present. Vasoactive peptides play no significant role in regulation of carp liver glycogenolysis.
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PMID:Hormonal regulation of hepatic glycogenolysis in the carp, Cyprinus carpio. 303 3

In vivo extracellular recordings from rat supraoptic and paraventricular magnocellular neurosecretory cells (MNCs) indicate that putative vasopressin-secreting MNCs may be identified by an abrupt and brief cessation in firing consequent to a transient drug-induced rise in arterial pressure sufficient to activate arterial baroreceptors. In the diagonal band of Broca (DBB), a population of neurons projecting towards the supraoptic nucleus are activated during this drug-induced hypertension. Electrical stimulation in DBB selectively depresses supraoptic vasopressin-secreting MNCs. Intracellular recordings in perfused hypothalamic explants confirm a DBB-evoked bicuculline-sensitive and chloride-dependent postsynaptic inhibition, similar to that associated with the application of gamma-aminobutyric acid (GABA) in approximately half of supraoptic MNCs. Since bicuculline also selectively blocks baroreceptor-induced inhibition in supraoptic MNCs, it is proposed that the depressant baroreflex input to vasopressin-secreting MNCs involves a population of DBB neurons and GABAergic interneurons located close to MNCs. An excitatory and selective input to vasopressin-secreting MNCs follows chemoreceptor activation, possibly mediated by the A1 noradrenergic cell group in the ventrolateral medulla. Another excitatory input to both vasopressin- and oxytocin-secreting MNCs is triggered by circulating angiotensin II and appears to be relayed centrally through an angiotensinergic projection from the subfornical organ.
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PMID:Cardiovascular input to hypothalamic neurosecretory neurons. 304 23

We previously reported that the rat posterior pituitary contains a potent PRL-releasing factor (PRF) which is distinct from oxytocin (OT), TRH, and angiotensin II (AII). The objectives of this study were 1) to examine whether posterior pituitary extracts stimulate PRL release in the presence of dopamine (DA), 2) to determine the chemical nature of PRF, and 3) to estimate its mol wt. Perifused anterior pituitary cells were used to assess PRF activity. Posterior pituitaries and medial basal hypothalamus (MBH) fragments were extracted with perchloric acid and lyophilized. Subsequent to various treatments, samples were reconstituted in the perifusion medium and introduced to the cells in short pulses. Fractions were collected and analyzed for hormone content by RIA. During a constant infusion of DA (50 nM), PRL secretion was inhibited by 75%, yet the posterior pituitary extract retained its ability to rapidly stimulate PRL release. Studies using proteolytic enzymes showed that posterior pituitary PRF was resistant to inactivation by trypsin, whereas the PRF activity of AII was abolished. Both chymotrypsin and proline-specific endopeptidase significantly reduced the PRF activity in the posterior pituitary. The PRL-releasing activity of TRH was not affected by chymotrypsin. Immunoreactive vasoactive intestinal polypeptide was undetectable in posterior pituitary extracts. Oxidation of posterior pituitary extracts with performic acid caused only a modest reduction of their PRF activity, while the ability of OT to stimulate PRL release as well as immunoreactive OT was abolished. Studies using ultrafiltration membranes showed that the PRF activity in the posterior pituitary was less than 5,000 mol wt. Furthermore, posterior pituitary PRF partitioned in nearly equal amounts across 1K membranes, as did AII and OT. In contrast, about 80% of the PRF activity in the MBH and all of the synthetic TRH passed through the 1K membranes. We conclude that 1) posterior pituitary PRF can stimulate PRL secretion from perifused anterior pituitary cells in the presence of physiological concentrations of DA; 2) PRF is a small peptide(s) of less than 5,000, and perhaps closer to 1,000, mol wt; 3) PRF is resistant to inactivation by trypsin and to oxidation by performic acid, but is hydrolyzed by both chymotrypsin and proline-specific endopeptidase; and 4) these data further distinguish posterior pituitary PRF from known PRL secretagogues.
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PMID:Characterization of prolactin-releasing factor in the rat posterior pituitary. 313 Nov 18

Calcium channel blockers inhibit myometrial contractility by preventing the increase in intracellular free calcium which follows stimulation. They could thus be useful in treating premature labour. The effect of nitrendipine, a dihydropyridine calcium channel antagonist, on the contractile response of strips of pregnant human myometrium to oxytocin, angiotensin II (AII) and ergometrine has been examined. A total of 68 tissue strips were studied, with random allocation to treatment group. Initial concentration: response curves to one of the three agonists were determined; the concentration:response determinations were repeated in the presence or absence of nitrendipine at 10(-9)M. The initial EC50S for tissues exposed to oxytocin and AII were 8.2 X 10(-10)M and 3.4 X 10(-8)M respectively. The contractile response to both agonists was significantly blunted in the presence of nitrendipine (ANOVA; P less than 0.001 for both agents). This effect was greatest at high agonist concentrations. The initial EC50S for tissues exposed to ergometrine was 3.9 X 10(-8)M. Exposure to nitrendipine blunted the response (ANOVA; P less than 0.001), an effect most marked at low concentrations of ergometrine. The effect of nitrendipine on myometrial responses to the naturally occurring hormones oxytocin and AII supports suggestions of a role for it in inhibiting premature labour.
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PMID:Studies on the effects of nitrendipine on oxytocin-, angiotensin II- and ergometrine-induced contraction of pregnant human myometrium in vitro. 316 51

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

The changes in plasma levels of arginine-vasopressin (AVP) and oxytocin (OXT) of rabbits by intraventricular administration of various drugs and their effects on the release of both hormones from the isolated posterior pituitary of rats were examined. An intraventricular injection of hypertonic saline, carbachol, angiotensin II, prostaglandin E2 or histamine to a rabbit increased the concentrations of plasma AVP and OXT, whereas serotonin decreased their plasma levels. Noradrenaline increased the concentration of OXT, but not that of AVP. Dopamine did not significantly affect the plasma level of either hormone. The release of AVP and OXT from the posterior pituitary fragments of rats was stimulated by changing the osmolality of the perfusion medium in vitro. Perfusion with medium containing dopamine suppressed the release of both hormones. However, the other bioactive amines and the drugs mentioned above did not affect the release of AVP and OXT.
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PMID:A study on the release mechanism of vasopressin and oxytocin. 323 19

We have examined the effects of systemic angiotensin II (AII) on plasma oxytocin (OXY) concentrations in freely moving male Sprague-Dawley rats. We have also examined the role of the subfornical organ (SFO) as a CNS site at which circulating AII acts to influence secretion of this neurohypophysial peptide. OXY concentrations were measured by radioimmunoassay in plasma samples obtained by drawing blood samples through indwelling atrial catheters. In SFO intact animals (n = 8) AII infusion (1.0 microgram/kg/min) resulted in increases in plasma OXY concentrations from baseline values of 6.8 +/- 2.5 pg/ml to postinfusion concentrations of 44.9 +/- 11.9 pg/ml. In a second series of experiments electrolytic lesions were placed in the region of the SFO prior to testing the effects of AII infusion on OXY concentrations. Two further experimental groups were thus established according to the histologically verified location of lesions in either the rostral or caudal SFO. In the caudal SFO lesioned group AII infusion resulted in increases in plasma OXY concentrations from control values of 6.9 +/- 1.4 pg/ml to postinfusion levels of 45.1 +/- 9.8 pg/ml. These changes were not significantly different from the SFO intact group. In contrast rostral SFO lesions resulted in significantly elevated basal concentrations of OXY (17.4 +/- 3.4 pg/ml, n = 6) while postinfusion concentrations were found to be 22.8 +/- 4.9 pg/ml indicating that AII infusion was without effect following such lesions. These data are in accordance with the hypothesis that circulating AII acts at the SFO to influence SFO efferents which in turn activate OXY secreting neurons in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei. These neuroendocrine cells then release this peptide into the systemic circulation from the posterior pituitary.
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PMID:Angiotensin acts at the subfornical organ to increase plasma oxytocin concentrations in the rat. 323 55

The effect of GnRH upon uterine contractions of both non-pregnant and pregnant rats was examined in vitro. In the non-pregnant rat uterus, GnRH inhibited in a concentration-and-time dependent manner the contractions induced by acetylcholine and oxytocin, but not those caused by bradykinin and angiotensin II. GnRH also inhibited the rhythmic contractions induced by oxytocin in uterine strips from late pregnant rats. These findings show that GnRH has a direct inhibitory effect on the rat uterine contractions, suggesting that GnRH-like substances may exert modulatory influences upon rat uterine contractility.
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PMID:Inhibitory effect of GnRH on isolated rat uterine muscle contractility. 329 Jun 5


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