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)

Following immobilization stress the supraoptic nucleus exhibits an increased number of coarse, heavily immunostained fibers in the basal glia labyrinth. Ultrastructural immunocytochemistry demonstrates a labeling of the rough endoplasmic reticulum in the neurosecretory perikarya and granule-free, immunoreactive material in the axons adjacent to the basal glia labyrinth. Furthermore, a labeling of the intercellular clefts of the neuropil is demonstrable in the supraoptic nucleus. These results lead to the hypothesis that 1) vasopressin is synthesized and released in two forms, in a granule-bound form and in a granule-free, probably more soluble form, and that 2) the latter might be released already in the nuclear area into the intercellular clefts from where it may reach its target cells via the cerebrospinal fluid of the subarachnoid space.
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PMID:Indication for a granule-free form of vasopressin in immobilization-stressed rats. 37 84

Ultrastructural examination of the posterior pituitary of the garden dormouse (Eliomys quercinus L) was carried out at different times in the annual cycle of this hibernating rodent. Obvious differences between experimental groups have not been observed, and the results presented here must be considered as general features of the garden dormouse posterior pituitary. Neurosecretory axons and endings can be divided into two types, according to different aspects of neurosecretory granules (NSG) and microvesicles (MV). One type contains spherical NSG with homogeneous cores and round MV. In the other type, NSG have various, often elongated, shapes. Their content shows two types of crystalline structures and most of the MV have flattened aspects. As it is very unlikely that this duality in NSG is a result of an artefact of fixation, three hypotheses are presented as explanation. The duality of NSG might be related either to their hormonal content (oxytocin or vasopressin) or to their degree of maturation. Moreover, both explanations may be valid. In the species studied, pituicytes often contain concentric lamellar structures of the endoplasmic reticulum (whorls), the significance of which remains obscure.
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PMID:The posterior pituitary of the garden dormouse (Eliomys quercinus l.). Evidence of two types of neurosecretory axons on the basis of ultrastructural characteristics. 64 48

Evolution of the (arginine)-vasopressin (AVP) content of the supraoptic (SON), paraventricular (PVN) and suprachiasmatic nuclei (SchN) and of the posterior lobe of the hypophysis (PLH) has been studied in rats at successive stages of rehydration after 4 days deprivation of drinking water. Particular attention has been focussed on short periods of rehydration. Evolution of the AVP content of the hypothalamo-posthypophysial system (HHS), the blood serum AVP concentration and osmolalities of serum and urine were compared. Variations of the AVP content in the different hypothalamo-hypophysial structures, are parallel. A marked depletion of AVP is observed after 2 and 4 days of dehydration. The AVP content of the PLH and of the hypothalamic nuclei shows two dramatic and short increases 15 min and 3 h after the onset of rehydration; these results are discussed in relation to the known physiological regulation mechanism of the HHS. In the PLH depleted by dehydration, reloading with neurosecretory granules (NSG) begins to be noticeable only after 24 h of rehydration, so that it does not seem to account for elevations of the AVP content occurring earlier. These could be related to a marked increase of the smooth endoplasmic reticulum (SER) network taking place in axons and nerve endings before the NSG reloading.
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PMID:Evolution of vasopressin levels in the hypothalamo-posthypophysial system of the rat during rehydration following water deprivation. Correlation with ultrastructural aspects in the posterior lobe. 73 44

Light microscopic observations using Nomarski optics on the aldehyde-fixed hypothalamus of normal adult cats, monkeys and rabbits revealed the presence of cells in the supraoptic, paraventricular and periventricular nuclei which possessed yellow birefringent inclusions. Immunogold labelling showed that in each species the cells displayed oxytocin-like immunoreactivity, both in electron-dense inclusions within some (but not all) cisterns of rough endoplasmic reticulum and in secretory granules. The cells in cats and rabbits were in all respects indistinguishable from the homologous 'birefringent' cells previously described in rats, but in monkeys, cells frequently contained additional inclusions in cisterns of rough endoplasmic reticulum which did not display oxytocin or vasopressin-like immunoreactivity, even after trypsin, pepsin or chymotrypsin treatment of sections. Observations on cats and rabbits using fluorescence microscopy revealed that the birefringent cells possessed bright autofluorescence which facilitated the identification of more cells than were seen using Nomarski optics alone. Autofluorescence was abolished when sections were mounted in glycerol, or when exposed to light for protracted periods of time. Attempts to label for monoamines in these cells were not successful, suggesting that the fluorescence is not due to aldehyde-induced amine fluorescence. It is not clear why neuropeptides are retained in some rough endoplasmic reticulum cisterns. It is possible that these birefringent cells contain a peptide, or peptides, which are abnormal in some manner, or which may be other members of the oxytocin gene family. Alternatively, the processing of neuropeptides to permit their export to the Golgi apparatus may be deficient. Acetylcholinesterase (AChE) histochemistry revealed that, unlike other oxytocin neurons, cells with intracellular accretions lacked detectable acetyl cholinesterase. As AChE is a known peptidase, it may be involved in regulating peptide export from the rough endoplasmic reticulum.
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PMID:Neuropeptide accretions in the endoplasmic reticulum of oxytocinergic neurons in cats, monkeys and rabbits: a widespread phenomenon. 129 66

We have previously reported that a component of ADP-evoked Ca2+ entry in human platelets appears to be promoted following the release of Ca2+ from intracellular stores. Other agonists may employ a similar mechanism. Here we have further investigated the relationship between the state of filling of the Ca2+ stores and plasma membrane Ca2+ permeability in Fura-2-loaded human platelets. Ca2+ influx was promoted following store depletion by inhibitors of the endoplasmic reticulum Ca(2+)-ATPase, thapsigargin (TG) and 2,5-di-(t-butyl)-1,4-benzohydroquinone (tBuBHQ). Divalent cation entry was confirmed by quenching of Fura-2 fluorescence with externally added Mn2+. It has been suggested that cytochrome P-450 may couple Ca2+ store depletion to an increased plasma membrane Ca2+ permeability. In apparent agreement with this, Mn2+ influx promoted by TG and tBuBHQ, or by preincubation of cells in Ca(2+)-free medium, was inhibited by the imidazole antimycotics, econazole and miconazole, which inhibit cytochrome P-450 activity. Agonist-evoked Mn2+ influx was only partially inhibited by these compounds at the same concentration (3 microM). Econazole (3 microM) reduced the Mn2+ quench evoked by ADP by 38% of the control value and that evoked by vasopressin, platelet activating factor (PAF) and thrombin no more than 15% of control, 20 s after agonist addition. Stopped-flow fluorimetry indicated that econazole had no detectable effect on the early time course of agonist-evoked Mn2+ entry or rises in [Ca2+]i. These data confirm the existence of a Ca2+ entry pathway in human platelets which is activated by depletion of the intracellular Ca2+ stores. Further, the results support the suggestion that cytochrome P-450 may participate in such a pathway. However, any physiological role for the cytochrome or its products in agonist-evoked events appears to be in the long-term maintenance or restoration of store Ca2+ content, rather than in promoting Ca2+ influx in the initial stages of platelet Ca2+ signal generation.
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PMID:Calcium influx evoked by Ca2+ store depletion in human platelets is more susceptible to cytochrome P-450 inhibitors than receptor-mediated calcium entry. 133 9

Effects of dehydration on vasopressin-secreting cells (VP cells) of the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) in the Mongolian gerbils were studied immunocytochemically and morphometrically. The plasma osmolality was measured at the time of sacrifice of individual animals and the body weight was measured every day during dehydration. The plasma osmolality increased significantly on day 3 of dehydration, followed by a gradual increase to reach nearly its equibilium state on day 10. The body weight decreased rapidly until day 10, followed by a gradual decrease thereafter. The area of VP cells increased significantly in both the SON and PVN on day 1 of dehydration, the level being nearly the same until days 3 to 5 and going up on day 7 to reach the plateau after day 15. These findings seem to reflect a compensation mechanism between the volume of body fluid and the plasma osmolality and to reflect responses of VP cells to the osmotic stimuli. Electron microscopic observation revealed that, at the beginning and late stages of dehydration, the increase in the area of VP cells was in parallel with the expansion of the Golgi area and with the distension of cisternae of the rough endoplasmic reticulum.
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PMID:Immunocytochemical and morphometric studies on the effects of dehydration on vasopressin-secreting cells in the hypothalamus of the Mongolian gerbils. 142 May 69

Magnocellular neurones in the supraoptic nuclei of normal Long Evans and homozygous Brattleboro rats were examined electron-microscopically after intracisternal injections of tunicamycin, puromycin, or brefeldin A. Moderate (50 micrograms) or high (200 micrograms) doses of tunicamycin caused the formation of electron-dense filamentous accretions in the endoplasmic reticulum (ER) cisterns of vasopressin neurones, but only the high dose of tunicamycin also caused accretions to form in the ER of some oxytocin neurones. Immunogold labelling of ultrathin sections from tunicamycin-treated rats revealed that, in about 5% of vasopressin neurones, the accretions could be immunogold-labelled for vasopressin and its associated neurophysin. However, in the majority of vasopressin neurones, the sections required trypsinisation before immunolabelling of the accretions could be detected. Small accretions in the ER of oxytocin neurones did not label for oxytocin or its neurophysin without prior trypsinisation, whereas larger accretions in other oxytocin cells could be labelled without prior trypsin treatment. Administration of puromycin resulted in the formation of small ER accretions in both vasopressin and oxytocin neurones. These accretions were immunolabelled with antisera, respectively, to vasopressin and oxytocin, but neurophysin-immunoreactivity was in most cases absent and was not revealed by treatment with trypsin, suggesting that neurophysin-immunoreactive epitopes were absent from truncated peptides forming the accretions. Brefeldin A caused dilatation of ER cisterns and disruption of the Golgi apparatus in both oxytocin and vasopressin neurones, but did not cause accretions to form in the ER.
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PMID:Tunicamycin, puromycin and brefeldin A influence the subcellular distribution of neuropeptides in hypothalamic magnocellular neurones of rat. 142 14

In homozygous Brattleboro rats a frame-shift mutation in the vasopressin gene prevents secretion of vasopressin by magnocellular neurosecretory neurons and thus causes diabetes insipidus. Whereas most "vasopressin" neurons in Brattleboro homozygotes apparently lack vasopressin and its associated neurophysin and glycopeptide, some isolated cells overcome the mutation and "revert" to producing readily detectable amounts of vasopressin. We describe here two morphologically and immunocytochemically distinct subsets of such "revertant" cells. One subset contain, in their rough endoplasmic reticulum cisterns, electron-dense aggregates immunoreactive for vasopressin, for parts of oxytocin-neurophysin, and for CP14 (a peptide with a sequence deduced from the mutated precursor), but not for vasopressin-associated glycopeptide ("glycopeptide") or vasopressin-neurophysin. In Brattleboro heterozygotes, which have one mutant and one normal copy of the vasopressin gene, morphologically similar revertant cells exist; the aggregates in the rough endoplasmic reticulum of these cells do not immuno-label for CP14, but the cells do produce 160-nm neurosecretory granules immunoreactive for vasopressin, vasopressin-neurophysin and glycopeptide. In Brattleboro homozygotes, the second, more abundant subset of neurons which recover vasopressin immunoreactivity also express vasopressin-associated glycopeptide and CP14 but not oxytocin-neurophysin; both glycopeptide and CP14 are restricted to the rough endoplasmic reticulum but do not form aggregates. We conclude that two different somatic repairs of the Brattleboro mutation can occur. We propose that, in aggregate-containing neurons, exons B and C have been exchanged between the vasopressin and oxytocin genes; glycopeptide-immunoreactive neurons have either undergone mismatch repair or exchanged exon B.
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PMID:Immuno-electron microscopic evidence for two different types of partial somatic repair of the mutant Brattleboro vasopressin gene. 143 2

The monohydroxy bile acid taurolithocholate (TLC) causes a rapid and transient increase in free cytosolic Ca2+ concentration ([Ca2+]i) in suspensions of rat hepatocytes similar to that elicited by the InsP3-dependent hormone vasopressin. The effect of the bile acid is due to a mobilization of Ca2+, independent of InsP3, from the endoplasmic reticulum (ER). Short-term preincubation of cells with the phorbol ester 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA), which activates protein kinase C (PKC), blocked the increase in [Ca2+]i induced by TLC, but did not alter that mediated by vasopressin. We obtained the following results, indicating that the effect of PMA is mediated by the activation of PKC. (1) Phorbol esters were effective over a concentration range where they activate PKC (IC50 = 0.5 nM); (2) phorbol esters that do not activate PKC did not inhibit the effects of TLC; (3) the permeant analogue oleoylacetylglycerol mimicked the inhibitory effect of PMA; (4) lastly, the inhibition of the TLC-induced Ca2+ mobilization by phorbol esters was partially prevented by preincubating the cells with the PKC inhibitors H7 and AMG-C16. Preincubating hepatocytes with PMA had no effect on the cell uptake of labelled TLC, indicating that the phorbol ester does not interfere with the transport system responsible for the accumulation of bile acids. In saponin-treated liver cells, PMA added before or after permeabilization failed to abolish TLC-induced Ca2+ release from the ER. The possibility is discussed that PMA, via PKC activation, may alter the intracellular binding or the transfer of bile acids in the liver.
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PMID:Taurolithocholate-induced Ca2+ release is inhibited by phorbol esters in isolated hepatocytes. 144 48

Experiments were designed to characterize the hormone sensitive transport of Ca2+ from the external media into rat hepatocytes maintained in culture. In the absence of added vasopressin, hepatocytes were nearly impermeable to Ca2+, whereas a significant and rapid influx of Ca2+ could be detected when external Ca2+ was added to hepatocytes after the addition of 20 nM vasopressin. The transport was measured as the initial rate of increase of free intracellular Ca2+ [( Ca2+]i) after Ca2+ addition to the external media. Most data were obtained from the majority of cells on a coverslip immersed in a spectrophotometric cuvette, but selected data were obtained by measuring Ca2+ changes in single cells. Ca2+ influx measured using a large number of cells was similar to data obtained using single cells. The Vmax of Ca2+ influx was 140 nM/s. Ca2+ transport was competitive with H+ so that the Km was 17.4 mM at pH 6.8, 3.7 mM at pH 7.4 and 1.8 mM at pH 7.8. Ca2+ influx was insensitive to external K+ (1 to 70 mM) and to the presence of 5 nM valinomycin, suggesting that it was independent of the electrical potential gradient across the plasma membrane. Transport also appeared to be insensitive to the activity of protein kinase C, which was varied by addition of the activator, 12-myristate 13-acetate phorbol ester, and by addition of the kinase inhibitor, staurosporine. Stimulation of transport following vasopressin addition exhibited a delay with a t1/2 of approximately 30 s. A vasopressin antagonist blocked the activation of transport, if added prior to vasopressin. However, experiments designed to determine the effect of hormone occupancy per se on transport activity indicated that continued hormone occupancy was not required. When the external medium was nominally Ca2+ free and an antagonist was added 1 min after vasopressin, Ca2+ entry, even 8 min after antagonist addition, was rapid. Conversely, preincubation with vasopressin antagonist in medium containing 0.5 mM Ca2+ dramatically lowered plasma membrane Ca2+ permeability. The ER Ca2+ pool emptied by vasopressin was refilled in the presence of vasopressin antagonist plus 0.5 mM Ca2+, but did not refill when the medium contained no added Ca2+. Under the conditions of these experiments, the Ca2+ levels of the ER hormone-sensitive Ca2+ pool were estimated as well as intracellular concentrations of inositol-1,4,5-trisphosphate. The Ca2+ levels of the endoplasmic reticulum correlated inversely with plasma membrane Ca2+ permeability, whereas cellular concentrations of inositol-1,4,5-trisphosphate did not correlate with Ca2+ permeability.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Regulation of plasma membrane permeability to calcium in primary cultures of rat hepatocytes. 165 96


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