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)

The rate of cutaneous water uptake after dehydration was significantly depressed in functionally neurohypophysectomized toads (Bufo marinus), which consequently regained weight much more slowly than intact toads when returned to water. Toads bearing hypothalamic lesions were able to develop an antidiuresis when removed from water to a saturated atmosphere, but the antidiuresis was solely glmerular in origin and was established more slowly than in intact animals. The fractional reabsorption of filtrate increased significantly and the relative free water clearance decreased significantly in intact toads after removal from water. These changes in tubular function, which were not seen in lesioned toads, were responsible for the development of a more rapid and effective antidiuresis in intact animals. Injections of iso-osmotic saline, oxytocin (250 mu./100 g) and vasopressin (50 mu./100 g) had no significant effect on rates of cutaneous water uptake in both intact and lesioned toads. Injections of hyperosmotic saline, however, significantly increased rates of water uptake in both groups of toads, but to a much greater extent in the intact animals. Fluid retention arising from a marked antidiuresis occurred after the injection of vasopressin and hyperosmotic saline, and there was some evidence of an antidiuretic effect of oxytocin with the doses used here. These results and their bearing on the question of the functional significance of the neurohypophysis in anuran amphibians are discussed.
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PMID:Effect of hypothalamic lesions on water metabolism of the toad Bufo marinus. 41 67

Intravenous injection of 20 International Units (IU) of oxytocin in the form of synthetic oxytocin or neurohypophyseal extract preparations to dehydrated cows that had already undergone twelve hours of water withdrawal did not produce antidiuresis but rather rise of diuresis accompanied by saluretic effects. Increase in diuresis occurred also in hyperhydrated cows, following water application, provided that oxytocin or vasopressin preparations had caused antidiuresis and saluresis and, consequently, changed urine composition to osmotic pressures beyond the limit values between 650 and 750 mosmol/kg. Rehydration of cow may be associated with retardation of diuresis by four hours or more. If oxytocin or vasopressin are given in the phase of such rehydration, the period between water application and the onset of water diuresis may be defined as "blocked water diuresis". Continuous infusion of 0.34 or 0.8 IU of oxytocin per minute up to 3.5 hours did not cause water intoxication in hyperhydrated cows, though blood plasma values for osmotic pressure had dropped to 244 mosmol/kg, while Na+ concentration had gone down to 116 mmol/l.
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PMID:[Studies of the induction of diuresis increase and water intoxication induced diuresis inhibition by oxytocin and vasopressin in lactating cattle]. 54 13

Since impurities consisting of neurohypophysical hormones in prolactin powder may be responsible for the vascular and renal effects attributed to prolactin, rat (NIH-RP-1), ovine (NIH-P-S-10, S-12), and bovine (NIH-P-B4) prolactin preparations were examined for their content of ADH and oxytocin by rat antidiuresis, milk-ejection, and blood pressure assays. Activities were identified as due to ADH or oxytocin by incubation of prolactin solutions with antisera against ADH, oxytocin, and prolactin, or with pregnancy plasma. The ADH content of rat, ovine (P-S-10, P-S-12) and bovine prolactin was found to be 104.5 +/- 7.1 (means +/- SE), 2.5 +/- 0.2, 1.6 +/- 0.1, and 1.6 +/- 0.5 mU/mg powder, respectively; the corresponding values for oxytocin content were 155.3 +/- 3.5, 1.2 +/- 0.1, 0.5 +/- 0.1, and 1.2 +/- 0.01 mU/mg powder, respectively. Because antidiuretic, milk-ejection, and blood pressure activities of the various prolactins were eliminated after incubation with antisera against ADH and oxytocin, or with pregnancy plasma, but not with prolactin antisera, it is concluded that the reported vascular and renal prolactin effects are attributable to ADH contamination of the prolactin preparation rather than to the prolactin molecule itself. These findings have implications for renal and vascular prolactin research.
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PMID:Contamination of prolactin preparations by antidiuretic hormone and oxytocin. 56 96

The distribution and properties of nonapeptide binding sites in the kidney of the anuran Xenopus laevis were investigated using quantitative in vitro autoradiography. The binding studies were performed with [3H]arginine vasopressin (AVP) as ligand because [125I]arginine vasotocin (AVT) lacks biological activity. Specific binding sites for [3H]AVP are located in the glomeruli of the kidney. [3H]AVP binding results in a steady state of association and dissociation between ligand and binding sites. Scatchard and Hill analyses of saturation experiments showed that [3H]AVP binds to a single class of binding sites with a dissociation constant (Kd) of 430 +/- 109 pM and a maximum binding capacity (Bmax) of 5.306 +/- 1.379 fmol/mm2 (n = 8). Displacement studies demonstrated the same affinity of these [3H]AVP binding sites to [3H]AVP, unlabeled AVP, and AVT, whereas mesotocin possesses only weak affinity. Further nonapeptides like oxytocin and isotocin or the mammalian-specific V1 receptor antagonist [1-beta-mercapto-beta,beta-cyclopentamethylene propionic acid)-2-(O-methyl)-tyrosine)-AVP or the V2 receptor agonist (1-deamino-8-D-arginine)-vasopressin or unrelated peptides did not alter the binding of [3H]AVP. The localization of nonapeptide binding sites in the glomeruli with the same affinity to AVP as to AVT agrees with the finding that AVT causes antidiuresis in Xenopus laevis. An earlier study demonstrated Xenopus laevis interrenal tissue to possess a higher sensitivity for AVT than AVP which points to a nonapeptide receptor with a higher affinity for AVT than AVP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Localization and quantification of nonapeptide binding sites in the kidney of Xenopus laevis: evidence for the existence of two different nonapeptide receptors. 156 20

Vasopressin action in the renal collecting duct is believed to be mediated by the cycling of water channels in principal and, possibly, intercalated cells. We used 6-carboxyfluorescein (6-CF) or fluorescein-labeled dextran (FITC-dextran) to determine the location and water permeability of endocytic vesicles from papilla and inner stripe of Brattleboro rats in different states of diuresis. Fifteen minutes after FITC-dextran infusion, fluorescent vesicles were concentrated at the apical pole of principal and intercalated cells. The osmotic water permeability (Pf) of these endosomes was measured by fluorescence quenching. In papillary endosomes, Pf was high (0.04 +/- 0.004 cm/s) when rats were in physiological states of antidiuresis or after treatment with vasopressin, 1-desamino-8-D-arginine vasopressin (DDAVP), or oxytocin; endosomes isolated from these regions of untreated animals had a low Pf. The number of papillary endosomes with high Pf increased with increasing doses of DDAVP. Endosomes from the inner stripe also had a high Pf only after vasopressin treatment. Confocal microscopy of sections of papilla showed that vasopressin significantly increased endocytosis in principal cells but had no effect on intercalated cells. Our data demonstrate that the bulk of fluorescently labeled vesicles from the papilla originate from the apical membrane of principal cells and contain water channels in their limiting membrane only when the rats are in physiological states of antidiuresis. In contrast, the majority of endocytosis in intercalated cells is not involved in water channel recycling.
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PMID:Endocytosis of water channels in rat kidney: cell specificity and correlation with in vivo antidiuresis. 170 69

Neurohypophysial secretion of vasopressin (AVP) and oxytocin (OT) was studied in rats maintained under hyposmolar conditions for 10-24 days. Graded intravenous infusions of hypertonic saline solutions had no consistent effect on plasma AVP and OT levels until plasma sodium concentration ([Na+]) exceeded 130 mM, after which levels of both hormones increased as an exponential function of plasma [Na+]. Detectable increases in plasma AVP and OT began at significantly lower plasma [Na+] in hyposmolar rats than in normosmolar control rats (10.8 mM lower for AVP and 18.4 mM lower for OT). AVP and OT secretion in hyposmolar rats was also markedly blunted in response to nonosmotic stimuli, including acute and chronic hypovolemia and systemic administration of cholecystokinin. Cessation of 1-desamino-8-D-arginine vasopressin-induced antidiuresis resulted in an appropriately rapid correction of plasma [Na+] to normal levels within 24 h. Consequently, although chronic hyposmolarity caused a moderate downward resetting of the osmotic thresholds for AVP and OT secretion, it did not cause sustained deficits in osmoregulation. These results suggest that osmoreceptor activity is regulated to maintain extracellular fluid and plasma osmolality within narrow absolute ranges rather than responding to relative changes in osmolality.
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PMID:Vasopressin and oxytocin secretion in chronically hyposmolar rats. 192 21

Arginine vasopressin (AVP) acts on at least two receptor types, classified on the basis of their second messengers. The V1 receptor acts via mobilization of intracellular calcium through phosphatidylinositol hydrolysis and influences blood pressure and hepatic glycogenolysis. The V2 receptor acts via cAMP through activation of adenylate cyclase and causes antidiuresis. Previous studies of the different AVP receptors have been hampered by the use of nonselective radioligands, such as [3H]AVP (which binds to all types of V1 and V2 receptors, certain oxytocin receptors, and neurophysins) as well as the difficulty of measurement of second messengers. This paper describes the use of selective V1 and V2 radioligands with in vitro autoradiography to study V1 and V2 binding sites in rat tissues. [125I][1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 7-sarcosine] arginine vasopressin ([125I][d(CH2)5,Sarcosine7]AVP), a selective V1 antagonist radioligand, bound to regions of the brain, testis, superior cervical ganglion, liver, blood vessels, and renal medulla. Pharmacological characterization of [125I][d(CH2)5,Sarcosine7]AVP binding was consistent with that expected for binding to V1 receptors. There was no specific binding demonstrable to pituitary, renal glomeruli, gut, heart, spinal cord, ovary, adrenal medulla, or adrenal cortex. [3H]1-deamino [8-D-arginine] vasopressin [( 3H]DDAVP), a potent V2 receptor agonist radioligand, was used to study V2 receptors. Specific binding was only identified in the kidney consistent with the known distribution of antidiuretic V2 receptors on renal collecting tubules. No binding was demonstrated on endothelium or liver where DDAVP might influence clotting factor release, nor in the brain, spinal cord, sympathetic ganglia, heart or vascular smooth muscle, regions where DDAVP might cause vasodilatation. These studies demonstrate the use of these radioligands to study V1 and V2 receptors in a variety of tissues. Also, since these ligands are selective they are of particular use to study the different receptor subtypes in tissues where V1 and V2 receptors coexist, such as in the kidney.
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PMID:Localization of vasopressin binding sites in rat tissues using specific V1 and V2 selective ligands. 230 15

The acute effects of physiological levels of AVP and oxytocin administration on renal water and sodium handling have been investigated in New Zealand genetically hypertensive and normotensive rats. AVP infusion was associated with an antidiuresis in both normotensive and hypertensive rats and while normotensive rats also displayed a dose-related natriuresis, this was attenuated in hypertensive rats. Oxytocin administration had no effect on urine flow or sodium excretion in normotensive rats, but was associated with an antidiuresis in hypertensive rats. Combined hormone infusion produced a greater reduction in urine flow than following AVP alone in both normotensive and hypertensive groups and was associated with a potentiation of the natriuretic action of AVP in the hypertensive animals. The data suggest that the contribution of oxytocin to renal sodium excretion in hypertensive rats may be suppressed. A compensatory increase in basal AVP secretion in hypertensive rats may overcome their apparent renal insensitivity to AVP, to maintain appropriate sodium excretion. This intriguing disturbance in neurohypophysial function may reflect or possibly contribute to the hypertension of these animals.
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PMID:Neurohypophysial hormone influence on renal function in the New Zealand genetically hypertensive rat. 339 74

Using implanted minipumps it was shown over a period of 7 days that the vasopressin antagonist, 1-deamino-pentamethylene-2-D-Phe-4-Ile-arginine vasopressin, caused increased diuresis in normal rats and reversed vasopressin- or oxytocin-induced antidiuresis in Brattleboro rats. When the antagonist was infused alone in Brattleboro rats it induced a marked antidiuretic response, indicating that the analogue also possessed agonistic properties. The agonist action could not be demonstrated in anaesthetized, hydrated normal rats. In these animals the analogue behaved as a pure antagonist. It is concluded that analogues which behave as antagonists in one test model may display agonistic properties under different experimental conditions.
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PMID:Antidiuretic antagonism and agonism of 1-deamino-pentamethylene-2-D-phenylalanine-4-isoleucine-arginine vasopressin in rats with diabetes insipidus. 355 52

1. Renal function and the effect of neurohypophysial hormone replacement was investigated in anaesthetized, acutely hypophysectomized, male rats. 2. Although urine production was only slightly lower over the 8 h post-operative study period in hypophysectomized rats, sodium excretion was greatly depressed reaching only 3.5 +/- 1.4 mumol/min compared with a peak of 13.2 +/- 1.0 mumol/min in intact animals. 3. In association with a decline in mean arterial blood pressure, glomerular filtration rate in hypophysectomized rats fell to 2.1 +/- 0.2 ml/min 8 h after operation by comparison with a mean rate in intact rats of 3.2 +/- 0.2 ml/min. 4. Plasma corticosterone levels were much lower in hypophysectomized (4 +/- 2 ng/ml) than in intact (36 +/- 4 ng/ml) rats, plasma aldosterone was reduced to a lesser extent (0.41 +/- 0.08 compared with 0.76 +/- 0.04 ng/ml). While oxytocin was not detectable in hypophysectomized rat plasma, trace levels of vasopressin (0.16 +/- 0.04 mu u./ml) were found. In intact unanaesthetized rats basal plasma levels of oxytocin were 0.32 +/- 0.13 mu u./ml and vasopressin were 0.85 +/- 0.19 mu u./ml. 5. Administration of oxytocin at 150 mu u./min, which produced plasma hormone levels (24.0 +/- 2.5 mu u./ml) greatly in excess of basal concentrations, increased renal sodium excretion but did not alter urine flow. Oxytocin administration at the lower rate of 15 mu u./min producing plasma hormone levels of 2.60 +/- 0.1 mu u./ml, did not alter renal sodium excretion. 6. Arginine vasopressin administered at 12 mu u./min induced plasma hormone levels of 1.54 +/- 0.09 mu u./ml and produced a large antidiuresis and small increase in the rate of sodium excretion. 7. The natriuretic response to vasopressin was potentiated by concurrent administration of oxytocin at 15 mu u./min. The peak sodium excretion of 5.8 +/- 1.0 mumol/min, however, remained well below that seen in intact rats. 8. It is concluded that, as restoration of posterior pituitary hormones at or above the physiological range only partially restored sodium excretion, the absence of anterior pituitary factors may also contribute directly or indirectly to the renal sodium retention of the hypophysectomized rat.
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PMID:The influence of neurohypophysial hormones on renal function in the acutely hypophysectomized rat. 362 41


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