Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The molecular weight of porcine neurophysin was estimated by molecular sieve chromatography and by analytical ultracentrifugation and was found to be in the order of 13,000.2. Internal evidence for the homogeneity of the preparation of neurophysin with respect to molecular weight was obtained in the ultracentrifugation experiments.3. The frictional ratio of neurophysin was 1.1 which suggests that the molecular form of the protein approximates to a sphere.4. The molecular weight and frictional ratio were not affected by temperature change (10-34 degrees C) or by twofold change in protein concentration.5. The binding of [(14)C]lysine vasopressin to porcine neurophysin was studied at 0, 27 and at 45 degrees C, and double reciprocal plots of the binding were shown to be curvilinear at 27 and at 45 degrees C and rectilinear at 0 degrees C.6. Concordant estimates for maximum binding capacity were obtained by extrapolations from the data at 27 and 45 degrees C by applying two independent empirical methods of approximation; these agreed with the estimate obtained by extrapolation of the straight line, fitting data obtained at 0 degrees C, being approximately 1 mole lysine vasopressin per 13,000 g protein.7. The association constant and thermodynamic parameters of the reaction were estimated for near saturation conditions. The reaction is entropy driven.8. The binding of lysine vasopressin was found to be dependent on protein concentration. No dependence of oxytocin binding on protein concentration was apparent.
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PMID:The molecular dimensions of porcine neurophysin and some thermodynamic parameters of the reaction with lysine vasopressin. 577 52

The effects of vanadate on cardiovascular function and on the secretion of renin and vasopressin were investigated by infusing sodium orthovanadate (0.32 mu mole/kg X min) intravenously into five conscious dogs. Vanadate caused significant increases in mean arterial pressure, total peripheral resistance, pulmonary arterial pressure, and cardiac output. These data illustrate that the hemodynamic effects of vanadate in the conscious dog are similar to those of the anesthetized dog but that minor differences do exist. Vanadate significantly suppressed plasma renin activity, but plasma vasopressin was unchanged. The effects of vanadate also were investigated in the same dogs on another day after administration of the calcium channel blocker, verapamil (0.3 mg/kg bolus + 0.01 mg/kg X min). After calcium channel blockade, the increases in arterial pressure and pulmonary arterial pressure induced by vanadate were attenuated, and cardiac output did not increase. Calcium channel blockade also prevented the vanadate-induced decrease in plasma renin activity. These data suggest that the cardiovascular and humoral alterations produced by vanadate in the conscious dog are at least partially mediated by changes in intracellular calcium.
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PMID:Cardiovascular and renin responses to vanadate in the conscious dog: attenuation after calcium channel blockade. 636 50

Toad bladders exposed to vasopressin (ADH) and then fixed on the mucosal surface with 1% glutaraldehyde were highly permeable to water and to urea compared to control bladders fixed in the absence of hormone. When identical conditions of fixation were were used, but the concentration of glutaraldehyde was decreased to 0.25%, the ADH-induced increase in membrane permeability to urea was preserved whereas water permeability was not. About 74% of the hormone-induced urea permeability sites were preserved by glutaraldehyde and were stable to changes in temperature as suggested by a constant value for the activation energy of urea movement of 5.4 kcal/mole (4-33 degrees C). In other studies bladders were exposed at low temperatures to 0.17% glutaraldehyde applied either to the serosal or the mucosal surface. The ADH-induced increase in membrane permeability to urea, bulk water, and tritiated water was well preserved with serosal fixation, but not with mucosal fixation. The observation that the urea pathway can be selectively preserved with 0.25% glutaraldehyde applied to the mucosa indicates that this structure is more accessible and (or) more sensitive to low-dose glutaraldehyde than is the ADH-induced water pathway. The observation that glutaraldehyde is more effective in stabilizing the ADH-induced urea channels from the serosal than from the mucosal surface indicates that these channels are not fixed at the extracellular surface of the apical plasma membrane. It appears, rather, that glutaraldehyde exerts its effects from an intracellular position, where it cross-links components of the urea channels at the cytoplasmic surface of the apical membrane and (or) inactivates the intracellular machinery responsible for the removal or dispersal of the ADH-induced urea permeability sites.
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PMID:Selective fixation with glutaraldehyde of ADH-induced urea permeability sites in toad bladder. 640 46

1. The effects of hyponatraemia on cerebral blood flow, oxidative metabolism, and transfer of Na and K from the brain--c.s.f. compartment to blood have been examined in anaesthetized calves 2--6 weeks after birth. 2. Dilutional hyponatraemia was produced by administration of a long-acting antidiuretic hormone analogue (desmopressin) and the infusion of hexose solutions of various concentrations. Cerebral blood flow was measured using a hydrogen clearance technique, and metabolism and cation transfer quantified by simultaneous determination of arterio-cerebral venous concentration differences. 3. Sustained hyposmolar hyponatraemia (plasma osmolality, 232 +/- 1 m-osmole/kg; plasma Na, 117 . 1 +/- 0 . 5 m-mole/l.) was associated with a fall in cerebral blood flow, and increase in measured net transfer of K from the brain-c.s.f. compartment to the circulation. C.s.f. Na concentration and osmolality were both decreased. 4. No alterations in these variables occurred during sustained isosmolar hyponatraemia (plasma osmolality, 284 +/- 2 m-osmole/kg; plasma Na, 119 . 9 +/- 0 . 2 m-mole/l). 5. The results are discussed in relation to the route, mechanism and time course of K loss from brain during hyponatraemia.
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PMID:Potassium transfer from brain to blood during sustained hyponatraemia in the calf. 746 70

Epidermal nevus syndrome is seldom encountered, and its association with hypermelanosis and the chronic syndrome of inappropriate antidiuretic hormone secretion (SIADH) has never been reported. A male neonate who developed intractable seizures and hyponatremia soon after birth is reported. He had alopecic patches on the scalp at birth. Large areas of skin hyperpigmentation, and epidermal nevi developed gradually. The clinical picture of hypotonic hyponatremia, high urine osmolality, elevated urine sodium, and euvolemia was compatible with SIADH. The seizures did not correlate with the hyponatremia, and no other cause for the seizures could be identified. The hyponatremia became chronic and was treated with a direct supply of sodium chloride. The development of the patient was markedly delayed at the last visit when he was 1 year of age. It is suggested that hypermelanosis and chronic SIADH may also be a variant presentation of epidermal nevus syndrome.
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PMID:Epidermal nevus syndrome with hypermelanosis and chronic hyponatremia. 1073 24

We have shown previously that histaprodifen and its Nalpha-substituted analogues methylhistaprodifen and dimethylhistaprodifen are highly potent H1-receptor agonists in vivo. The aim of the present study was to examine the influence of four newly synthesized histaprodifen analogues, 3-fluoro-methylhistaprodifen (1), Nalpha-imidazolylethylhistaprodifen (2), bis-histaprodifen (3) and Nalpha-methyl-bis-histaprodifen (4), on the cardiovascular system in the pithed and in the anaesthetized rat. In pithed and vagotomized rats, diastolic blood pressure (which was increased to 80-85 mmHg by vasopressin infusion) was decreased dose dependently by methylhistaprodifen (the reference compound) and by compounds 1-4. The maximum decrease was about 47-50 mmHg for methylhistaprodifen and compounds 1, 2 and 3. Their potencies, expressed as pED50 (the negative logarithm of the dose in mole per kilogram body weight that decreased diastolic blood pressure by 25 mmHg), were 8.31, 8.23, 8.26 and 7.84, respectively. With compound 4 the maximal effect was not achieved at doses up to 1 micromol/kg (the latter dose decreased blood pressure by about 30 mmHg; pED50 approximately 6.5). The vasodepressor effect of the five compounds was attenuated by the H1-receptor antagonist dimetindene (1 micromol/kg) but was not changed by combined administration of the H2- and H3-receptor antagonists ranitidine and thioperamide (1 micromol/kg each), by combined administration of the alpha1- and alpha2-adrenoceptor antagonists prazosin and rauwolscine (1 micromol/kg each) or by the beta-adrenoceptor antagonist propranolol (3 micromol/kg). In anaesthetized rats methylhistaprodifen and compounds 1-4 induced almost the same fall in blood pressure as in pithed and vagotomized animals; the effects were sensitive to blockade by dimetindene (1 micromol/kg). Higher doses of compounds 1 and 2 (1 micromol/kg) increased heart rate in pithed and vagotomized rats in a manner sensitive to propranolol (3 micromol/kg) but insensitive to dimetindene (3 micromol/kg). The same dose of methylhistaprodifen and of compounds 3 and 4 failed to affect heart rate. We conclude that the agonistic potency of compounds 1 and 2 at H1-receptors in the cardiovascular system of the rat equals that of methylhistaprodifen, the most potent histamine H1-receptor agonist available until recently. Compounds 1 and 2 exhibit sympathomimetic activity at high doses.
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PMID:Novel histaprodifen analogues as potent histamine H1-receptor agonists in the pithed and in the anaesthetized rat. 1148 33

An attempt has been made to assess the validity of applying the frictional and viscous coefficients of bulk water to the movement of water and solutes through the urinary bladder of the toad. The temperature dependence of diffusion of THO, C(14)-urea, C(14)-thiourea, and net water transfer across the bladder was determined in the presence and absence of vasopressin. The activation energy for diffusion of THO was 9.8 kcal per mole in the absence of vasopressin and 4.1 kcal per mole with the hormone present. Activation energies simultaneously determined following vasopressin for diffusion and net transfers of water were similar, and in the same range as known activation energies for diffusion and viscous flow in water. Urea had activation energies for diffusion of 4.1 and 3.9 kcal per mole in the absence and presence of vasopressin, respectively. Thiourea had a high activation energy for diffusion of 6.3 kcal per mole, which was unchanged, 6.6 kcal per mole, following hormone. These findings suggest that in its rate-limiting permeability barrier, water is present in a structured state, offering a high resistance to penetration by water. Vasopressin enlarges the aqueous channels so that the core of water they contain possesses the physical properties of ordinary bulk water. Urea penetrates the tissue via these aqueous channels while thiourea is limited by some other permeability barrier.
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PMID:The state of water in the isolated toad bladder in the presence and absence of vasopressin. 1390 90

Neurophysin-M, a methionine-containing protein that is the major constituent of neurophysin, has been crystallized as complexes with [8-arginine]-vasopressin. Three moles of vasopressin alone or 2 moles of vasopressin together with 1 mole of oxytocin are bound/mole of protein. An amorphous complex of the protein with oxytocin alone contains 2 moles of the hormone/mole of protein. Deamino-[8-arginine]-vasopressin, a highly active basic analogue of vasopressin, is not bound by neurophysin. The primary amino group of both vasopressin and oxytocin is necessary for binding with neurophysin.
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PMID:The composition of crystalline complexes of neurophysin-M with [8-arginine]-vasopressin and oxytocin. 1674 66

Naked mole-rats are eusocial rodents that live in large subterranean colonies in which one queen breeds with one to three males. All other animals are nonbreeding subordinates. The external features of male and female subordinates, including their genitalia, are remarkably monomorphic, as is their behavior. Because vasopressin (VP) is associated with social behaviors and sex differences in other species, its distribution in naked mole-rats was of interest. We used immunohistochemistry to examine VP in the brains of subordinate and breeding naked mole-rats of both sexes. As in other mammals, VP-immunoreactive (-ir) somata were found in the paraventricular (PVN) and supraoptic nuclei (SON) and VP-ir projections from these nuclei ran through the internal and external zone of the median eminence. However, naked mole-rats had very few VP-ir cells in the bed nucleus of the stria terminalis (BST) and none in the suprachiasmatic nucleus (SCN); the extensive network of fine-caliber VP-ir fibers usually seen in projection sites of the BST and SCN were also absent. Equally unexpected was the abundance of large-caliber VP-ir fibers in the dorsomedial septum. VP immunoreactivity was generally similar in all groups, with the exception of VP-ir cell number in the dorsomedial hypothalamus (DMH). Breeders had a population of labeled cells in the DMH that was absent, or nearly absent, in subordinates. Future studies on the function of VP in these areas are needed to determine how the atypical distribution of VP immunoreactivity relates to eusociality and the unusual physiology of naked mole-rats.
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PMID:Distribution of vasopressin in the brain of the eusocial naked mole-rat. 1718 41

Purification of 125I-labelled lysine-vasopressin has been achieved by affinity chromatography on a Sepharose 4 B conjugate of porcine neurophysins. This affinity absorbent did not retain halogenated hormone, while native lysine-vasopressin was bound on the solid support. The specific activity of purified iodinated lysine-vasopressin was 1700-1800 Ci/g, corresponding to one iodine atom per mole. By comparison with an unpurified tracer, a five times increase in the minimum detectable dose was obtained in the vasopressin radioimmunoassay.
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PMID:Purification of 125I-labelled lysine-vasopressin by affinity chromatography on sepharose-bound neurophysins. 1999 41


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