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)

Swiss mouse 3T3 fibroblasts were grown in tissue culture, fixed with lysine-paraformaldehyde-periodate solutions containing 0 to 0.1% Tween 20, and then stained for cyclooxygenase antigenicity using rabbit anti-cyclooxygenase IgG in the peroxidase anti-peroxidase procedure. When examined by light microscopy, those cells fixed in the presence of 0.03 to 0.1% Tween 20 exhibited staining throughout the cytoplasm and around the nucleus but not on the cell surface. No staining occurred when either preimmune IgG or anti-cyclooxygenase IgG adsorbed with purified enzyme was substituted for the immune IgG. Electron microscopic examination of cells treated with fixative containing 0.05% Tween 20 and then stained for cyclooxygenase antigenicity revealed electron-dense deposits on the endoplasmic reticulum and nuclear membrane but not the mitochondrial or plasma membranes. No staining was seen in cells treated with control sera. Agents such as angiotensin II, bradykinin, antidiuretic hormone, and thrombin interact, apparently with the 3T3 cell surface to cause a release of arachidonic acid and prostaglandin E2 formation (Pong, S.S., Hong, S. L., and Levine, L. (1977) J. Biol. Chem. 252, 1408-1413). Our results establish that conversion of arachidonic acid to the prostaglandin endoperoxide precursor of PGE2 actually takes place on the endoplasmic reticulum and the nuclear envelope.
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PMID:Subcellular localization of prostaglandin-forming cyclooxygenase in Swiss mouse 3T3 fibroblasts by electron microscopic immunocytochemistry. 676 26

This study concerns the timing and magnitude of exocytosis and endocytosis in the granular cells of toad bladder during the hydroosmotic response to antidiuretic hormone. Granule exocytosis at the luminal cell surface is extensive within 5 min of the administration of a physiological dose of hormone. Hydroosmosis becomes detectable during this time period. The amount of membrane added to the luminal surface by exocytosis during 60 min of exposure to hormone can be of the same order of magnitude as the extent of the luminal plasma membrane. Endocytosis, demonstrated by peroxidase uptake from the luminal surface, becomes extensive during the period 15-45 min after hormone administration. Thus, maximal endocytic activity occurs later than the period of most extensive exocytosis and seems to correlate with the onset of the decline in water movement. The amount of membrane retrieved from the luminal surface by endocytosis during 60 min of stimulation is at least three quarters of that added by exocytosis. The bulk membrane movement in ADH stimulated preparations does not require the presence of an osmotic gradient. Colchicine inhibits the hydroosmotic response, the exocytosis of granules, and endocytosis at the luminal surface. These results strengthen our view that the bulk circulation of membrane at the cell surface, via exocytosis and endocytosis, is closely related to the permeability changes occurring at the surface.
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PMID:Quantitative analysis of exocytosis and endocytosis in the hydroosmotic response of toad bladder. 677 96

Vasopressin, oxytocin and neurophysin were localized in the brains and spinal cords of four primates (tree shrew, squirrel monkey, rhesus monkey and human) using antisera to these peptides and the unlabelled antibody-enzyme peroxidase antiperoxidase method. Magnocellular neurons in the hypothalamus stained positively for vasopressin, oxytocin or neurophysin. Parvocellular neurons of the suprachiasmatic nucleus (SCN) stained positively for vasopressin and neurophysin but not for oxytocin, in all four species. Magnocellular oxytocin, vasopressin and neurophysin neurons project to permeable capillaries in the neurohypophysis, as well as to various extrahypothalamic neural target areas including the central amygdala, nucleus of the solitary tract, dorsal motor nucleus of the vagus, lateral reticular nucleus, dorsal horn, central grey and intermediolateral nucleus of the spinal cord. In target areas, terminals contact somata and dendrites. Parvocellular vasopressin and neurophysin neurons of the SCN do not project to the neurohypophysis, and project only to neural target areas, including the lateral septum, mediodorsal thalamus, lateral habenula, mesencephalic central grey, medial amygdala and ventral hippocampus. (Due to the relatively poor tissue preservation in human autopsy specimens not all projections found in the other primates could be confirmed in humans.) These findings confirm and correlate well with previous descriptions made in rodents, and indicate that vasopressin, oxytocin and neurophysin projections to neural targets are present in primates. Peptides released from these projections probably do not enter the bloodstream, but are rather involved in neural mechanisms.
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PMID:Immunohistochemistry of vasopressin, oxytocin and neurophysin in the hypothalamus and extrahypothalamic regions of the human and primate brain. 678 43

In order to study the morphological relationship between the dopaminergic and the vasopressinergic endings in the rat posterior pituitary, a combination of radioautography and immunocytochemistry techniques was applied to the same ultrathin section of the posterior pituitary. Immunocytochemical localization (peroxidase-antiperoxidase technique) of vasopressin was first applied, followed by the radioautography detection of [3H] dopamine that had been injected 30 and 60 min before fixation. This double labeling technique has established that the dopaminergic endings that contain both dense core vesicles (60-100 nm in diameter) and small clear vesicles are always found in close proximity to vasopressinergic neurosecretory endings, suggesting an interaction between these two systems. This relatively easy approach should be very useful to study the connections between different neurotransmitter systems in the nervous system.
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PMID:Identification of ending containing dopamine and vasopressin in the rat posterior pituitary by a combination of radioautography and immunocytochemistry at the ultrastructural level. 682 86

The distribution of gonadotropin-releasing hormone (GnRH) was studied in the brain and infundibulum (INF) or median eminence of sheep utilizing a peroxidase-antiperoxidase immunohistochemical method. This procedure utilized a specific antiserum generated against GnRH conjugated to bovine serum albumin. In the rostral INF, the greatest concentration of GnRH positive axons was found in the medial region, mostly in the external layer dorsal to the hypophysial portal plexus. In the intermediate portion of the INF, the hormone was mainly observed in the external layer at the more dorsolateral areas ventral to the tuberoinfundibular sulcus. GnRH was generally located medially in the caudal portion of the INF and dorsomedially in the rostral infundibular stalk. Substantial amounts of reaction product were also noted in the internal layer throughout the entire rostrocaudal extent of the INF. The hormone was localized in axons throughout the brain from the septal and medial preoptic areas to the mammillary bodies. GnRH-positive perikarya were scattered in various regions of the infundibular (arcuate) and for the first time in the ventromedial nuclei of sheep hypothalamus. Preabsorption of the specific antiserum with synthetic GnRH abolished staining in both axons and perikarya, whereas preabsorption with thyrotropin-releasing hormone, oxytocin, arginine-vasopressin, and adrenocorticotrophic hormone did not affect staining intensity.
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PMID:Immunohistochemical localization of gonadotropin-releasing hormone (GnRH) in the brain and infundibulum of the sheep. 701 81

When sections through rat neurohypophyses were treated with trypsin prior to incubation with enkephalin antibodies, vasopressin terminals invariably exhibited leucine-enkephalin-like immunoreactivity. Omitting tryptic cleavage the vasopressin terminals of some specimens only were immunostained. The enkephalin-like material was contained in the neurosecretory granules as shown by the protein A gold and the peroxidase anti-peroxidase method. We assume that the leucine-enkephalin sequence in vasopressin endings to some extent is present in a precursor form, possibly as dynorphin or alpha-neo-endorphin, from which the pentapeptide is liberated by enzymatic cleavage.
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PMID:Leucine-enkephalin-like immunoreactivity in vasopressin terminals is enhanced by treatment with peptidases. 715 32

The vasopressin system of the rat was examined in the course of the first 12 h of rehydration after prolonged thirst at light and elctron microsscopic levels and by use of the peroxidase anti-peroxidase (PAP) method. Light microscopically, the median eminence was the only part of the system that not only displayed distinct differences between animals of different rehydration times but also showed a characteristic pattern of immunohistochemical reactivity in its rostro-caudal distribution. Ultrastructurally, in the perikarya a maximal labeling of the rough endoplasmic reticulum was observed after 2 h of rehydration, whereas an extensive labeling of the enlarged Golgi zones was attained after 4 h of resupplying water. A labeling of the intercellular clefts in the basal glial labyrinth of the supraoptic nucleus (and to a lesser degree in the subependymal neuropil adjacent to the paraventricular nucleus) was increased 30 min after the onset of drinking, as compared with water-deprived animals; it decreased slightly after 12 h of rehydration. The filling of the swollen fibers by increasing amounts of labeled axoplasmic reticulum, evident in the nuclear areas already after 30 min of water supply, begins in the median eminence after 2 h of rehydration and is fully developed after 4 and 8 h. Corresponding results hold true for the neural lobe but are somewhat delayed in comparison to the findings in the median eminence. The discussion considers (i) synthesis and transport of nongranular vasopressin within the axoplasmic reticulum, and (ii) release not only from the neural lobe but also from the nuclear areas and from the fibers of the median eminence.
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PMID:Nongranular vasopressin synthesis and transport in early stages of rehydration. 738 14

1. The effects of Na+ on vasopressin release and on redistribution of Ca2+, Na+ and H+ in isolated rat neurohypophysial nerve endings have been studied. 2. Substituting Na+ for a non-permanent cation produced a pronounced and sustained release of vasopressin. This increase occurred in the absence of external Ca2+ and in nerve endings loaded with the Ca2+ chelator dimethyl-BAPTA (1,2-bis-(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid). 3. The effect of Na+ was independent of a rise in intracellular Ca2+ as judged by the measurement of [Ca2+]i using the indicator fura-2 and 45Ca2+ efflux studies. Although Na+ could release Ca2+ from internal reservoirs the small elevation in [Ca2+]i induced by Na+ could not explain the large and sustained increase in vasopressin secretion. 4. The channel blockers TTX (tetrodotoxin), D888 (desmethyoxyverapamil), N144 (5-nitro-2-(phenylpropylamino)-benzoic acid) or SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonic acid) could not prevent the Na(+)-dependent increase in vasopressin release. Similarly this increase was not affected by metabolic inhibitors (Ruthenium Red and KCN) nor by CCCP (carbonyl cyanide m-chlorophenylhydrazone), an uncoupler of oxidative phosphorylation. 5. Selectivity among monovalent cations to promote secretion was found with the largest effect on the secretory response being produced by Na+. Similarly Cl- was found to be the most potent anion studied for inducing, in the presence of Na+, an increase in neurohormone release. 6. Measuring [Na+]i by means of the Na+ indicator SBFI showed that the extent of the secretory response was correlated with the intraterminal Na+ concentration. 7. The Na(+)-induced, Ca(2+)-independent release of vasopressin occurred by exocytosis as judged (i) by the linear relationship between the amount of vasopressin secreted and that of the co-localized neurophysin and (ii) by the demonstration that the extracellular marker horseradish peroxidase was only found in endocytotic vacuoles and not in the cytoplasm of the stimulated nerve endings. 8. The Na(+)-dependent secretory response found on addition of extracellular Na+ was not the result of the change in internal pH as measured with the indicator BCECF and as mimicked by addition of propionic acid. 9. Addition of Na+ to digitonin- or streptolysin-O-permeabilized nerve endings in the presence or absence of Ca2+ also gave rise to an increase in vasopressin secretion. 10. It is concluded that an increase in internal Na+ per se can promote, in the absence of a rise in intracellular Ca2+, an increase in neuropeptide secretion.
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PMID:Sodium-evoked, calcium-independent vasopressin release from rat isolated neurohypophysial nerve endings. 750 28

The localisation and colocalisation of neuronal isoform (type I) nitric oxide synthase, endothelin-1, arginine-vasopressin and substance P in endothelial cells of rat coronary and femoral arteries was investigated by pre-embedding and postembedding immunocytochemistry. Nitric oxide synthase appeared in a high proportion of endothelial cells of both arteries (about 89% in the femoral artery, examined with the preembedding avidin-biotin-peroxidase method, and in almost all cells of the coronary artery, examined with the postembedding immunogold technique). Double immunogold labelling in single cells demonstrated the colocalisation of nitric oxide synthase with endothelin-1, arginine-vasopressin and substance P. The immunolabelling was mostly confined to the cytoplasmic matrix. It is suggested that nitric oxide synthase/nitric oxide and the peptides examined may be involved in local control of blood flow in coronary and femoral arteries.
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PMID:Localisation of nitric oxide synthase and its colocalisation with vasoactive peptides in coronary and femoral arteries. An electron microscope study. 752 54

Taurine is an inhibitory amino acid that hyperpolarizes magnocellular neurosecretory neurons. To determine which cell types in the rat supraoptic nucleus contain taurine, we used a monoclonal antibody raised against a taurine conjugate. Preembedding immunocytochemistry was carried out at the light and electron microscopic levels using diaminobenzidine and gold-substituted silver-intensified peroxidase as markers. We report the presence of taurine in all cellular compartments of the supraoptic nucleus, except axons, with variable labeling intensities among the different compartments. Few cell bodies of magnocellular neurons were immunoreactive, but many distal dendrites and some proximal ones showed weak-to-moderate levels of immunoreactivity. Strong immunoreactivity was found over glial cell bodies and their processes, in particular in the ventral glial lamina of the supraoptic nucleus. Large astrocytic processes labeled with the taurine antibody included the endfeet participating in the glial limitans around capillaries and at the ventral surface of the hypothalamus. Other types of immunoreactive astrocytic profiles were found scattered within the neuropil where these processes participated in different interactions with the neuronal elements of the supraoptic nucleus. Immunoreactive glial expansions, sometimes even the main process of the glial cell, engulfed axonal boutons. Other labeled glial processes were found between two magnocellular perikarya or closely apposed to the membrane of axonal boutons contacting the neuronal cell bodies. The frequent finding of closely apposed glial and dendritic elements bearing different levels of taurine-like immunoreactivity suggests that exchange of taurine between those two compartments may occur. We propose that taurine could be released from supraoptic glia by a small decrease in osmolarity or by receptor-mediated mechanisms during conditions of low hormonal (vasopressin and/or oxytocin) needs. Such released taurine could then act on presynaptic or postsynaptic sites, or both, to exert its neuromodulatory actions.
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PMID:Taurine immunoreactivity in the rat supraoptic nucleus: prominent localization in glial cells. 761 71


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