33 results on '"Oiso, Y"'
Search Results
2. Endoplasmic reticulum stress in vasopressin neurons of familial diabetes insipidus model mice: aggregate formation and mRNA poly(A) tail shortening.
- Author
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Arima H, Morishita Y, Hagiwara D, Hayashi M, and Oiso Y
- Subjects
- Animals, Diabetes Insipidus, Neurogenic genetics, Diabetes Insipidus, Neurogenic metabolism, Disease Models, Animal, Endoplasmic Reticulum genetics, Endoplasmic Reticulum metabolism, Endoplasmic Reticulum pathology, Humans, Hypothalamus metabolism, Hypothalamus pathology, Mice, Protein Folding, RNA, Messenger genetics, Vasopressins genetics, Diabetes Insipidus, Neurogenic pathology, Endoplasmic Reticulum Stress physiology, Neurons pathology, Vasopressins metabolism
- Abstract
The immunoglobulin heavy chain binding protein (BiP) is an endoplasmic reticulum (ER) chaperone, which binds to newly synthesized secretory and transmembrane proteins to facilitate protein folding. BiP mRNA is expressed in the arginine vasopressin (AVP) neurons in the supraoptic nucleus of wild-type mice even in basal conditions, and the expression levels increase in response to dehydration. These data suggest that AVP neurons are subjected to ER stress. Familial neurohypophysial diabetes insipidus (FNDI) is caused by mutations in the gene locus of AVP. The mutant proteins could accumulate in the ER and possibly increase ER stress in the AVP neurons. We bred mice possessing a mutation causing FNDI, which manifested progressive polyuria, as do the patients with FNDI. Electron microscopic analyses demonstrated that aggregates accumulated in the ER of AVP neurons in FNDI mice. Despite polyuria, which could potentially induce dehydration, AVP mRNA expression was decreased in the supraoptic nucleus, and the AVP mRNA poly(A) tail length was shortened in FNDI mice compared with wild-type mice. Incubation of hypothalamic explants of wild-type mice with ER stressors caused shortening of the poly(A) tail length of AVP mRNA, accompanied by decreases in the expression. These data revealed a mechanism by which ER stress decreases poly(A) tail length of AVP mRNA, and this reduces the load of unfolded proteins that form the aggregates in ER of the AVP neurons in FNDI mice.
- Published
- 2014
- Full Text
- View/download PDF
3. A marked difference in the vasopressin responsiveness between the adrenal glands in a patient with adrenocorticotropin-independent macronodular adrenal hyperplasia.
- Author
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Miyata M, Yoshida M, Shinoda J, Sasano H, and Oiso Y
- Subjects
- Adenoma pathology, Adenoma surgery, Adrenal Cortex metabolism, Adrenal Cortex pathology, Adrenal Cortex Neoplasms pathology, Adrenal Cortex Neoplasms surgery, Adrenalectomy, Adrenocorticotropic Hormone metabolism, Cushing Syndrome blood, Cushing Syndrome complications, Cushing Syndrome surgery, Deamino Arginine Vasopressin, Dexamethasone, Diabetes Mellitus, Type 2 etiology, Glucose Tolerance Test, Gonadotropin-Releasing Hormone, Humans, Hydrocortisone metabolism, Hypertriglyceridemia etiology, Laparoscopy, Male, Middle Aged, Organ Size, Thyrotropin-Releasing Hormone, Adenoma physiopathology, Adrenal Cortex drug effects, Adrenal Cortex Neoplasms physiopathology, Cushing Syndrome physiopathology, Receptors, Vasopressin drug effects, Vasopressins pharmacology
- Abstract
We herein present the case of a 53-year-old patient with adrenocorticotropin-independent macronodular adrenocortical hyperplasia (AIMAH), which is a rare form of Cushing syndrome. He had hypercortisolemia and bilateral macronodular adrenal glands with a left side predominance. The administration of vasopressin significantly increased the plasma cortisol level (1.9-fold). Following left adrenalectomy, the patient's hypercortisolemia significantly improved and vasopressin responsiveness was lost, suggesting that the responsiveness originated from the resected left adrenal gland. The marked difference in vasopressin responsiveness between the adrenals corresponded with their asymmetrical size and function. Evaluating the differences in the vasopressin sensitivity may therefore be helpful for understanding the progression of AIMAH.
- Published
- 2013
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4. BiP mRNA expression is upregulated by dehydration in vasopressin neurons in the hypothalamus in mice.
- Author
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Hagiwara D, Arima H, Morishita Y, Goto M, Banno R, Sugimura Y, and Oiso Y
- Subjects
- Animals, Corticotropin-Releasing Hormone genetics, Corticotropin-Releasing Hormone metabolism, Endoplasmic Reticulum Chaperone BiP, Heat-Shock Proteins genetics, Male, Mice, Mice, Inbred C57BL, Oxytocin genetics, Oxytocin metabolism, Paraventricular Hypothalamic Nucleus metabolism, Supraoptic Nucleus metabolism, Vasopressins genetics, Dehydration metabolism, Heat-Shock Proteins metabolism, Neurons metabolism, Paraventricular Hypothalamic Nucleus pathology, Supraoptic Nucleus pathology, Up-Regulation, Vasopressins metabolism
- Abstract
The immunoglobulin heavy chain binding protein (BiP) is an endoplasmic reticulum (ER) chaperone that facilitates the proper folding of newly synthesized secretory and transmembrane proteins. Here we report that BiP mRNA was expressed in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus in wild-type mice under basal conditions. Dual in situ hybridization in the SON and PVN demonstrated that BiP mRNA was expressed in almost all the neurons of arginine vasopressin (AVP), an antidiuretic hormone. BiP mRNA expression levels were increased in proportion to AVP mRNA expression in the SON and PVN under dehydration. These data suggest that BiP is involved in the homeostasis of ER function in the AVP neurons in the SON and PVN., (Copyright © 2012 Elsevier Inc. All rights reserved.)
- Published
- 2012
- Full Text
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5. [Vasopressin (AVP)].
- Author
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Murase T and Oiso Y
- Subjects
- Humans, Radioimmunoassay, Water-Electrolyte Imbalance blood, Vasopressins blood
- Published
- 2010
6. Vasopressin and oxytocin: focus in the post-genomic era.
- Author
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Brown CH, Oiso Y, and Ueta Y
- Subjects
- Humans, Genomics, Oxytocin physiology, Vasopressins physiology
- Published
- 2010
- Full Text
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7. Activation of vasopressin neurons leads to phenotype progression in a mouse model for familial neurohypophysial diabetes insipidus.
- Author
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Hiroi M, Morishita Y, Hayashi M, Ozaki N, Sugimura Y, Nagasaki H, Shiota A, Oiso Y, and Arima H
- Subjects
- Animals, Deamino Arginine Vasopressin pharmacology, Diabetes Insipidus, Neurogenic genetics, Disease Progression, Drinking drug effects, Drinking physiology, Hematocrit, Hypoglycemic Agents pharmacology, Immunohistochemistry, In Situ Hybridization, Male, Mice, Mice, Inbred C57BL, Osmolar Concentration, Phenotype, Sodium, Dietary pharmacology, Urodynamics drug effects, Vasopressins biosynthesis, Diabetes Insipidus, Neurogenic physiopathology, Neurons physiology, Pituitary Gland, Posterior physiopathology, Vasopressins physiology
- Abstract
Familial neurohypophysial diabetes insipidus (FNDI) is a rare disease that is inherited in an autosomal dominant manner. In a previous study, we made a mouse model for FNDI, which showed progressive polyuria accompanied by inclusion bodies in the arginine vasopressin (AVP) neurons formed by aggregates in the endoplasmic reticulum. The present study was conducted to determine whether the activities of AVP neurons are related to the phenotype progression in the FNDI model. In the first experiment, female heterozygous mice were administered either desmopressin (dDAVP) or a vehicle (control) subcutaneously with osmotic minipumps for 30 days. The dDAVP treatment significantly decreased the urine volume, AVP mRNA expression, and inclusion bodies in the AVP neurons. Urine volume in the dDAVP group remained significantly less than the control for 14 days even after the minipumps were removed. In the second experiment, the males were fed either a 0.2% Na or 2.0% Na diet for 6 mo. Urine AVP excretion was significantly increased in the 2.0% Na group compared with the 0.2% Na group for the first 2 mo but gradually decreased thereafter. Throughout the experiments, urine volume increased progressively in the 2.0% Na group but not in the 0.2% Na group. Immunohistochemical analyses revealed that inclusion bodies in the AVP cells had significantly increased in the 2.0% Na compared with the 0.2% Na group. These data demonstrated that activation of AVP neurons could accelerate the aggregate formation as well as the progression of the polyuria in the FNDI model mice.
- Published
- 2010
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8. Enhanced cardiovascular alteration and Fos expression induced by central salt loading in a conscious rat transgenic for the metallothionein-vasopressin fusion gene.
- Author
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Chu CP, Kato K, Jin QH, Qiu DL, Yu NS, Oiso Y, and Kannan H
- Subjects
- Animals, Animals, Genetically Modified, Antidiuretic Hormone Receptor Antagonists, Arginine genetics, Brain drug effects, Brain metabolism, Consciousness, Immunohistochemistry, Injections, Intraventricular, Male, Oncogene Proteins v-fos drug effects, Piperidines pharmacology, Quinolones pharmacology, Rats, Rats, Sprague-Dawley, Receptors, Vasopressin metabolism, Recombinant Fusion Proteins genetics, Sodium Chloride administration & dosage, Cardiovascular System drug effects, Metallothionein genetics, Oncogene Proteins v-fos biosynthesis, Saline Solution, Hypertonic administration & dosage, Vasopressins genetics
- Abstract
The present study is an investigation of the responses of the cardiovascular system and Fos expression to intracerebroventricular (i.c.v.) administration of hypertonic saline (HS) in conscious arginine vasopressin (AVP)-overexpressing transgenic (Tg) and control rats. Central HS (0.3, 0.67, or 1.0M NaCl, 1 microl/min for 20 min) significantly increased the mean arterial blood pressure (MABP) and Fos-like immunoreactivity (FLI) in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus, the area postrema (AP), the median preoptic nucleus (MnPO), and the organum vasculosum laminae terminalis (OVLT) in both Tg and control rats. The changes in MABP and FLI were significantly larger in Tg rats than in control rats. i.c.v. pretreatment with the AVP V1 receptor antagonist, OPC-21268, blocked the increase in MABP and significantly decreased the Fos expression in the PVN (posterior magnocellular (pm) component) induced by 0.3 M HS in the Tg rats. The present study demonstrates an increased responsiveness to i.c.v. administration of HS in AVP Tg rats, suggesting the relationship between the vasopressinergic drive and central cardiovascular response via, at least in part, the V1 receptor in the PVN magnocellular neurons.
- Published
- 2005
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9. Possible involvement of phosphatidylinositol 3-kinase/Akt signal pathway in vasopressin-induced HSP27 phosphorylation in aortic smooth muscle A10 cells.
- Author
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Suga H, Nakajima K, Shu E, Kanno Y, Hirade K, Ishisaki A, Matsuno H, Tanabe K, Takai S, Akamatsu S, Kato K, Oiso Y, and Kozawa O
- Subjects
- Animals, Blotting, Western, Cell Line, Chromones pharmacology, Enzyme Inhibitors pharmacology, HSP27 Heat-Shock Proteins, Imidazoles pharmacology, MAP Kinase Signaling System, Molecular Chaperones, Morpholines pharmacology, Muscle, Smooth, Vascular cytology, Phosphatidylinositol 3-Kinases metabolism, Phosphorylation, Piperidines pharmacology, Proto-Oncogene Proteins c-akt, Pyridines pharmacology, Quinolones pharmacology, Rats, Time Factors, Aorta metabolism, Heat-Shock Proteins metabolism, Muscle, Smooth metabolism, Myocytes, Smooth Muscle metabolism, Neoplasm Proteins metabolism, Phosphatidylinositol 3-Kinases physiology, Protein Serine-Threonine Kinases metabolism, Proto-Oncogene Proteins metabolism, Vasopressins pharmacology
- Abstract
We previously reported that p38 mitogen-activated protein (MAP) kinase takes a part in arginine vasopressin (AVP)-induced heat shock protein 27 (HSP27) phosphorylation in aortic smooth muscle A10 cells. In the present study, we investigated whether phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) is involved in the phosphorylation of HSP27 in these cells. AVP time-dependently induced the phosphorylation of PI3K and Akt. Akt inhibitor, 1l-6-hydroxymethyl-chiro-inositol 2-(R)-2-O-methyl-3-O-octadecylcarbonate, partially suppressed the phosphorylation of HSP27. The AVP-induced HSP27 phosphorylation was attenuated by LY294002, a PI3K inhibitor. The combination of Akt inhibitor and SB203580, a p38 MAP kinase inhibitor, completely suppressed the AVP-induced phosphorylation of HSP27. Furthermore, LY294002 or Akt inhibitor did not affect the AVP-induced phosphorylation of p38 MAP kinase and SB203580 did not affect the phosphorylation of PI3K or Akt. These results suggest that PI3K/Akt plays a part in the AVP-induced phosphorylation of HSP27, maybe independently of p38 MAP kinase, in aortic smooth muscle A10 cells.
- Published
- 2005
- Full Text
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10. [Genetic disorders of vasopressin and vasopressin receptor genes].
- Author
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Murase T and Oiso Y
- Subjects
- Humans, Diabetes Insipidus congenital, Receptors, Vasopressin genetics, Vasopressins genetics
- Published
- 2005
11. [Transgenic, knock-out and knock-in animal models for vasopressin neuron systems].
- Author
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Hayashi M, Arima H, and Oiso Y
- Subjects
- Animals, Mice, Rats, Rats, Brattleboro, Animals, Genetically Modified, Neurons chemistry, Vasopressins analysis
- Published
- 2005
12. Novel mutant vasopressin-neurophysin II gene associated with familial neurohypophyseal diabetes insipidus.
- Author
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Miyakoshi M, Kamoi K, Murase T, Sugimura Y, and Oiso Y
- Subjects
- Adult, Base Sequence, Deamino Arginine Vasopressin therapeutic use, Diabetes Insipidus, Neurogenic blood, Female, Humans, Hyponatremia genetics, Male, Middle Aged, Molecular Sequence Data, Neurophysins blood, Pedigree, Polyuria genetics, Protein Precursors blood, Sequence Analysis, DNA, Vasopressins blood, Diabetes Insipidus, Neurogenic genetics, Mutation, Missense, Neurophysins genetics, Protein Precursors genetics, Vasopressins genetics
- Abstract
We describe a novel missense mutant of arginine vasopressin (AVP)-dependent neurohypophyseal diabetes insipidus in an autosomal dominant family. A 54-year-old woman was admitted to our hospital because of thyroidectomy for thyroid cancer. After thyroidectomy she was found to have hypernatremia and polyuria and polydipsia both of which had been present from childhood. She had no obstructive hydronephrosis. Her father, father's younger sister and her third son also had polyuria and polydipsia. Basal plasma AVP concentration at normal plasma osmolality was normal but did not respond to increased plasma osmolality despite hyperosmolality during infusion of hypertonic saline infusion, indicating that plasma AVP secretion was impaired. Sodium concentration in urine and urine osmolality were low and increased after nasal administration of DDAVP. There was a diminished but bright signal of pituitary posterior gland on magnetic resonance T1 weighted image. Molecular genetic analysis demonstrated that the patient and her son had a single heterozygous missense mutation (G-->A) at nucleotide 1829 in 1 AVP allele, yielding an abnormal AVP precursor with lacking Glu-47 in its neurophysin II moiety. The abnormal AVP precursor may be related to the impaired AVP secretion.
- Published
- 2004
- Full Text
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13. Leukemia inhibitory factor stimulates vasopressin release in rats.
- Author
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Ishizaki S, Murase T, Sugimura Y, Banno R, Arima H, Miura Y, and Oiso Y
- Subjects
- Animals, Dose-Response Relationship, Drug, Leukemia Inhibitory Factor, Male, Rats, Rats, Sprague-Dawley, Interleukin-6 pharmacology, Vasopressins blood, Vasopressins metabolism
- Abstract
Leukemia inhibitory factor (LIF) is a cytokine of the interleukin-6 family exhibiting diverse physiological functions during inflammatory stress. It is well known that syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is often associated with inflammatory disease, and cytokines produced at inflammatory foci are thought to stimulate arginine vasopressin (AVP) release. In the present study, we investigated the effects of centrally administered LIF on AVP release in conscious rats. Intracerebroventricular administration of LIF (0.01-1.0 microg/rat) significantly increased the plasma AVP concentration, and its effect was observed from 5 to 60 min after the injection. LIF did not cause significant changes in plasma Na+, total protein and blood pressure. There were no significant changes in the plasma AVP concentration after intravenous injection of LIF (1.0, 3.0 microg/rat). These results indicate that LIF plays a stimulatory role in the regulation of AVP release, and suggest the possibility that LIF may be involved in the pathogenesis of SIADH.
- Published
- 2004
- Full Text
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14. Osmoregulation of vasopressin release and gene transcription under acute and chronic hypovolemia in rats.
- Author
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Kondo N, Arima H, Banno R, Kuwahara S, Sato I, and Oiso Y
- Subjects
- Acute Disease, Animals, Blood Proteins analysis, Chronic Disease, Gene Expression Regulation, Hypovolemia chemically induced, Male, Plasma Volume, Polyethylene Glycols, Rats, Rats, Sprague-Dawley, Sodium blood, Hypovolemia genetics, Hypovolemia metabolism, Transcription, Genetic, Vasopressins metabolism, Water-Electrolyte Balance
- Abstract
Although acute decreases in plasma volume are known to enhance the osmotically induced arginine vasopressin (AVP) release, it is unclear whether there is also such interaction at the level of gene transcription. It also remains to be established how sustained changes in plasma volume affect the osmoregulation. In this study, we examined how acute and chronic decreases in blood volume affected the osmoregulation of AVP release and gene transcription in rats. Acute hypovolemia was induced by intraperitoneal injection of polyethylene glycol (PEG), and chronic hypovolemia was induced by 3 days of water deprivation (WD) or 12 days of salt loading (SL). Rats were injected with isotonic or hypertonic saline, and plasma AVP levels and AVP heteronuclear (hn)RNA expression in the supraoptic and paraventricular nuclei, an indicator of gene transcription, were examined in relation to plasma osmolality in each group. Plasma AVP levels were correlated with plasma Na levels in all groups. Whereas the regression lines relating plasma AVP to Na were almost identical among control, WD, and SL groups, the thresholds of plasma Na for AVP release were significantly decreased only in the PEG group. AVP hnRNA levels were also correlated with plasma Na levels in control and PEG groups, and the thresholds were significantly decreased in the PEG group. In contrast, there was no significant correlation of AVP hnRNA and plasma Na levels in WD and SL groups. Thus it was demonstrated that acute and chronic reduction in plasma volume affected the osmoregulation of AVP release and gene transcription in different ways.
- Published
- 2004
- Full Text
- View/download PDF
15. Gene therapy for central diabetes insipidus: effective antidiuresis by muscle-targeted gene transfer.
- Author
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Yoshida M, Iwasaki Y, Asai M, Nigawara T, and Oiso Y
- Subjects
- Animals, COS Cells, Diuresis physiology, Furin, LLC-PK1 Cells, Male, Muscle, Skeletal cytology, Myoblasts physiology, Neurosecretory Systems physiology, Rats, Rats, Brattleboro, Swine, Transfection, Diabetes Insipidus, Neurogenic therapy, Genetic Therapy methods, Muscle, Skeletal physiology, Myoblasts transplantation, Vasopressins genetics
- Abstract
Central diabetes insipidus, characterized by severe polyuria and polydipsia, is a disorder resulting from deficient secretion of the small neuropeptide hormone vasopressin in the neurohypophysis. The standard therapy is daily and life-long administration of vasopressin analog (desmopressin acetate), but gene therapy is potentially alternative to the conventional replacement therapy. To obtain the therapeutic neuropeptide more feasibly, we tried to express vasopressin in nonneuronal tissues using nonviral gene transfer techniques. We found that the unprocessed large precursor form, provasopressin, was predominantly produced in nonendocrine cells transfected with the wild-type vasopressin gene, because of the lack of neuroendocrine cell-specific endopeptidases. In sharp contrast, appropriately processed bioactive vasopressin can be efficiently produced even in nonendocrine cells with a modified vasopressin gene containing a ubiquitous endoprotease furin cleavage site. We also succeeded in maintaining a long-term antidiuretic effect on vasopressin-deficient (Brattleboro) rats by direct introduction of the furin-processible gene into skeletal muscle by electroporation. Altogether, our data clearly show that skeletal muscle is a useful target tissue for continuous delivery of bioactive neuropeptide. Furthermore, our strategies may be applicable to future gene therapies for central diabetes insipidus and other peptide hormone deficiencies.
- Published
- 2004
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16. Regulation of vasopressin gene expression by cAMP and glucocorticoids in parvocellular neurons of the paraventricular nucleus in rat hypothalamic organotypic cultures.
- Author
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Kuwahara S, Arima H, Banno R, Sato I, Kondo N, and Oiso Y
- Subjects
- Animals, Colforsin pharmacology, Cyclic AMP pharmacology, Dexamethasone pharmacology, Gene Expression Regulation drug effects, In Situ Hybridization, In Vitro Techniques, Neurons drug effects, Paraventricular Hypothalamic Nucleus drug effects, RNA Stability drug effects, RNA Stability physiology, RNA, Messenger metabolism, Rats, Rats, Sprague-Dawley, Cyclic AMP physiology, Gene Expression Regulation physiology, Glucocorticoids pharmacology, Neurons metabolism, Paraventricular Hypothalamic Nucleus physiology, Vasopressins genetics
- Abstract
Arginine vasopressin (AVP) in the parvocellular neurons of the paraventricular nucleus (PVN) is known to play an important role in the hypothalamo-pituitary-adrenal axis. In the present study, we examined how cAMP and glucocorticoids regulate AVP gene expression in the parvocellular neurons of the PVN in rat hypothalamic organotypic cultures with in situ hybridization. AVP heteronuclear (hn) RNA, an indicator for gene transcription, was induced in the PVN with incubation of forskolin as reported previously, and AVP mRNA was increased by forskolin in the presence of the gene transcription inhibitor 5,6-dichloro-1-D-ribofuranosylbenzimidazole (DRB). These data indicate that cAMP could increase not only gene transcription but also mRNA stability. Dexamethasone treatment, in contrast, significantly decreased AVP mRNA expression levels in the PVN, but this inhibitory action was abolished in the presence of DRB or the sodium channel blocker tetrodotoxin (TTX). However, when the hypothalamic slices were treated with forskolin, dexamethasone decreased AVP mRNA expression even in the presence of DRB and/or TTX. Furthermore, AVP hnRNA expression induced by forskolin was attenuated by dexamethasone treatment in the presence of TTX. These data indicate that dexamethasone could act on AVP cells independently of action potentials to decrease mRNA stability and to suppress AVP gene transcription during stimulation by cAMP. Thus, it was demonstrated that: (1) cAMP upregulates AVP gene transcriptionally and post-transcriptionally, (2) the mode of action of glucocorticoids was dependent on whether the cells were stimulated by cAMP, and (3) the interactions between cAMP and glucocorticoids encompass both gene transcription and mRNA stability.
- Published
- 2003
17. Transgenic rat models of vasopressin overexpression.
- Author
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Oiso Y, Nagasaki H, and Yokoi H
- Subjects
- Animals, Animals, Genetically Modified, Disease Models, Animal, Down-Regulation, Humans, Rats, Receptors, Vasopressin genetics, Vasopressins biosynthesis, Vasopressins genetics
- Abstract
Vasopressin has an important role in water metabolism and its impairment induces some clinical disorders such as diabetes insipidus or syndrome of inappropriate antidiuresis (SIAD). SIAD is caused by the overproduction of vasopressin which induces diluting hyponatremia. The accurate diagnosis and appropriate therapy have not settled up to date because its pathophysiology is very complicated. It is meaningful to develop a rat model of SIAD in which human vasopressin gene is overexpressed in order to analyze pathophysiological changes. Several models transgenic for vasopressin including us had been generated. The transgenic rats provide a useful model to investigate various pathophysiological changes resulting from the oversecretion of vasopressin. Some interesting results based on these animal models are reviewed.
- Published
- 2003
18. Role of ghrelin in the regulation of vasopressin release in conscious rats.
- Author
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Ishizaki S, Murase T, Sugimura Y, Kakiya S, Yokoi H, Tachikawa K, Arima H, Miura Y, and Oiso Y
- Subjects
- Animals, Antibodies, Blocking pharmacology, Blood Pressure drug effects, Blood Proteins metabolism, Dose-Response Relationship, Drug, Ghrelin, Injections, Intravenous, Injections, Intraventricular, Kinetics, Male, Neurons drug effects, Neurons physiology, Neuropeptide Y antagonists & inhibitors, Neuropeptide Y physiology, Peptides administration & dosage, Rats, Rats, Sprague-Dawley, Sodium blood, Vasopressins blood, Peptide Hormones, Peptides pharmacology, Vasopressins metabolism
- Abstract
GH secretagogue (GHS) is a small, synthetic compound that has the potential to stimulate GH release via its specific receptors (GHS-R). Ghrelin is a novel 28-amino acid peptide recently isolated from human and rat stomach, and it is thought to be the endogenous ligand for GHS-R. Ghrelin has a variety of physiological functions such as the stimulation of GH release or the increase of food intake by activating NPY neurons. In the present study, we investigated the effects of ghrelin on AVP release in conscious rats. Intracerebroventricular (icv) administration of ghrelin increased the plasma AVP concentration in a dose-dependent manner (1-1000 pmol/rat), and its effect was observed as late as 60 min after the administration. Icv injection of ghrelin caused no significant change in plasma osmolality, plasma volume, or arterial blood pressure. Iv administration of ghrelin (10 nmol/rat) also increased the plasma AVP concentration, which was accompanied by a significant decrease in arterial blood pressure. Pretreatment with antiserum against NPY significantly reduced the plasma AVP increase induced by icv administration of ghrelin. These results suggest that ghrelin plays a stimulatory role in AVP release, which is possibly mediated by NPY neurons.
- Published
- 2002
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19. [Vasopressin and water metabolism].
- Author
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Oiso Y
- Subjects
- Animals, Vasopressins physiology, Water metabolism
- Published
- 1998
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20. Vasopressin and related disorders.
- Author
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Oiso Y and Iwasaki Y
- Subjects
- Arginine Vasopressin genetics, Arginine Vasopressin urine, Diabetes Insipidus diagnosis, Diabetes Insipidus genetics, Diabetes Insipidus urine, Humans, Mutation, Protein Precursors genetics, Vasopressins genetics, Vasopressins physiology
- Published
- 1998
- Full Text
- View/download PDF
21. Positive and negative regulation of the rat vasopressin gene promoter.
- Author
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Iwasaki Y, Oiso Y, Saito H, and Majzoub JA
- Subjects
- Animals, Base Sequence, Colforsin pharmacology, Cyclic AMP Response Element-Binding Protein genetics, Cyclic AMP Response Element-Binding Protein pharmacology, Cyclic AMP-Dependent Protein Kinases metabolism, Dexamethasone pharmacology, Gene Deletion, Gene Expression Regulation physiology, Glucocorticoids pharmacology, Humans, Molecular Sequence Data, Promoter Regions, Genetic drug effects, Promoter Regions, Genetic genetics, Protein Kinase C metabolism, Rats, Tumor Cells, Cultured, Promoter Regions, Genetic physiology, Vasopressins genetics
- Abstract
To study the transcriptional regulation of the vasopressin gene in vitro, 3 kb of the 5' regulatory region of the rat vasopressin gene was isolated and subcloned, along with a series of various deletion mutants, into vectors containing the luciferase reporter gene. After transfecting these genes transiently into the human choriocarcinoma cell line JEG-3 along with a glucocorticoid receptor (GR) expression vector, transcriptional activity was quantitated using the luciferase assay. Forskolin, 8-bromo-cAMP, and protein kinase A catalytic subunit expression all markedly increased transcription from the 3-kb promoter. Analyses with deletion mutants of the promoter showed that two cAMP-responsive element (CRE)-like sequences (-227 to -220 bp and -123 to -116 bp) contribute to this positive regulation. Expression of KCREB, a dominant negative mutant of the cAMP-responsive element binding protein (CREB), suggested the involvement of CREB. Transfection of the activator protein 2 (AP2) DNA consensus sequence partially blocked transcription. Dexamethasone suppressed forskolin-stimulated expression. The negative effect of glucocorticoid was GR dependent and may be mediated by a mechanism not involving GR binding to DNA because it was independent of the putative glucocorticoid-responsive element previously reported in the vasopressin promoter (-622 to -608 bp) and was preserved in the shorter promoter constructs in which no glucocorticoid-responsive element-like sequence was found. Our data suggest that several trans-acting factors including CREB, AP2, and GR are likely to be involved in vasopressin gene transcription and that the positive and negative regulation of vasopressin gene transcription is complex.
- Published
- 1997
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22. [Disorders of body water regulation and the therapy--water metabolism disorder and vasopressin].
- Author
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Oiso Y and Iwasaki Y
- Subjects
- Animals, Humans, Mutation, Diabetes Insipidus diagnosis, Diabetes Insipidus genetics, Inappropriate ADH Syndrome genetics, Vasopressins genetics
- Published
- 1997
23. Osmoregulation of plasma vasopressin in three cases with adrenal insufficiency of diverse etiologies.
- Author
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Iwasaki Y, Kondo K, Hasegawa H, and Oiso Y
- Subjects
- Adrenal Insufficiency drug therapy, Adrenal Insufficiency etiology, Adrenocorticotropic Hormone deficiency, Adult, Aged, Diabetes Insipidus complications, Female, Humans, Hydrocortisone therapeutic use, Hyponatremia, Hypopituitarism complications, Male, Pituitary Neoplasms complications, Polyuria, Vasopressins metabolism, Adrenal Insufficiency physiopathology, Vasopressins blood, Water-Electrolyte Balance
- Abstract
Neurohypophyseal function was studied by hypertonic saline infusion with plasma vasopressin measurement in 3 patients with adrenal insufficiency before and after cortisol replacement. Although each patient had different causes of adrenal insufficiency, all showed impaired water excretion before replacement. The first patient with isolated adrenocorticotropin deficiency had marked hyponatremia and inappropriate vasopressin secretion which was normalized after replacement, indicating vasopressin hypersecretion during hypoadrenocorticism. The second patient had combined anterior and posterior pituitary deficiency due to postpartum hypopituitarism and showed completely absent vasopressin secretion, with her polyuria being masked before cortisol replacement, suggesting a vasopressin-independent intrarenal mechanism of antidiuresis. The third patient with panhypopituitarism due to a pituitary tumor also had preexisting diabetes insipidus with defective vasopressin secretion. In this case, however, plasma vasopressin was found to be elevated when adrenal insufficiency and hyponatremia subsequently developed. Together, these results indicate that vasopressin hypersecretion does occur during adrenal insufficiency, but that the accompanying urinary diluting defect may be attributable either to vasopressin-dependent or to vasopressin-independent mechanisms.
- Published
- 1997
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24. Osmoregulation of plasma vasopressin in diabetes mellitus with sustained hyperglycemia.
- Author
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Iwasaki Y, Kondo K, Murase T, Hasegawa H, and Oiso Y
- Subjects
- Adult, Blood Glucose metabolism, Blood Glucose physiology, Female, Humans, Hypertonic Solutions, Male, Middle Aged, Sodium blood, Sodium Chloride administration & dosage, Diabetes Mellitus blood, Hyperglycemia blood, Vasopressins blood, Water-Electrolyte Balance
- Abstract
We studied osmoregulation of plasma vasopressin in 5 patients with newly diagnosed diabetes mellitus. All patients showed typical symptoms of uncontrolled diabetes mellitus such as marked hyperglycemia, polyuria, and polydipsia, but did not have advanced diabetic complications. Vasopressin release was studied using 5% hypertonic saline infusion test twice: before treatment when the patient was hyperglycemic, and after treatment 1 to 2 months later when the patient was euglycemic. Plasma vasopressin was measured by a sensitive and specific radioimmunoassay. The mean basal plasma vasopressin value in the patients was significantly higher in the hyperglycemic compared with the euglycemic state (3.75 +/- 0.70 vs 1.18 +/- 0.46 pmol/l, respectively; P < 0.05). The relationship of plasma vasopressin with serum sodium, but not plasma osmolality, during hyperglycemia showed an apparent hypersecretion of vasopressin. In both cases, the sensitivity of the vasopressin response to osmotic stimuli was significantly decreased. During euglycemia, the sensitivity of vasopressin secretion to either sodium or osmolality was almost normal, although a slight rise in the osmostat was observed compared with normal subjects. Together, we found that the positive correlation of vasopressin with sodium or osmolality is maintained but significantly altered in patients with untreated diabetes mellitus. Especially noteworthy is the lowered threshold and decreased sensitivity of osmotically-induced vasopressin secretion during hyperglycemia, which may be caused by multiple factors such as diabetes-associated hypovolemia, osmogenic effects of glucose and other osmoles, depletion of the pool of vasopressin available for release, and the metabolic derangement of osmoreceptor/magnocellular neurons.
- Published
- 1996
- Full Text
- View/download PDF
25. Vasopressin activates phospholipase D through pertussis toxin-insensitive GTP-binding protein in aortic smooth muscle cells: function of Ca2+/calmodulin.
- Author
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Miwa M, Kozawa O, Suzuki A, Watanabe Y, Shinoda J, and Oiso Y
- Subjects
- Animals, Aorta metabolism, Cells, Cultured, Enzyme Activation, Male, Pertussis Toxin, Rats, Rats, Sprague-Dawley, Signal Transduction, Virulence Factors, Bordetella, Calcium metabolism, Calmodulin metabolism, GTP-Binding Proteins metabolism, Muscle, Smooth, Vascular metabolism, Phospholipase D metabolism, Vasopressins pharmacology
- Abstract
In the present study, we examined the effect of vasopressin (AVP) on phosphatidylcholine-hydrolyzing phospholipase D activity in primary cultured rat aortic smooth muscle cells. AVP stimulation of choline formation was dose dependent. The time-course was quite different from those of inositol phosphates. The effect of AVP on the formation of inositol phosphates (EC50 was 3 nM) was more potent than that on the formation of choline (EC50 was 30 nM). 12-O-Tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C (PKC), stimulated the formation of choline. However, 4 alpha-phorbol 12,13-didecanoate, which is inactive for PKC, had little effect. Staurosporine, an inhibitor of protein kinases, which inhibited the TPA-induced formation of choline, had little effect on the AVP-induced formation of choline. Neither calphostin C, a highly specific PKC inhibitor, nor PKC down-regulation with TPA affected AVP-induced formation of choline. A combination of AVP and TPA additively stimulated the formation of choline. The depletion of extracellular Ca2+ by (ethylenebis(oxyethylenenitrilo)tetraacetic acid significantly reduced the AVP-induced formation of choline. W-7, an antagonist of calmodulin, inhibited the AVP-induced formation of choline in a dose-dependent manner. NaF, an activator for GTP-binding protein (G-protein), stimulated the formation of choline. However, the formation of choline by a combination of AVP and NaF was not additive. Pertussis toxin had little effect on the AVP-induced formation of choline.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1995
- Full Text
- View/download PDF
26. Glucocorticoid amplifies vasopressin-induced phosphoinositide hydrolysis in aortic smooth muscle cells.
- Author
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Watanabe Y, Tokuda H, Suzuki A, Shinoda J, Kotoyori J, Ito Y, Oiso Y, and Kozawa O
- Subjects
- Animals, Aorta, Thoracic drug effects, Cells, Cultured, Drug Synergism, Enzyme Activation, Feedback, Hydrolysis, Inositol 1,4,5-Trisphosphate biosynthesis, Male, Muscle, Smooth, Vascular cytology, Muscle, Smooth, Vascular metabolism, Protein Kinase C drug effects, Rats, Rats, Sprague-Dawley, Dexamethasone pharmacology, Muscle, Smooth, Vascular drug effects, Phosphatidylinositols metabolism, Vasopressins pharmacology
- Abstract
It has been reported that glucocorticoid modifies phosphoinositide (PI) hydrolysis stimulated by vasoactive agents in vascular smooth muscle cells. In the present study, we investigated the point at which glucocorticoid affects vasopressin-induced PI hydrolysis in primary cultured rat aortic smooth muscle cells. The pretreatment with dexamethasone significantly amplified the formation of inositol trisphosphate (IP3) induced by vasopressin in a dose-dependent manner in a range of 1 pM to 10 nM. The effect of dexamethasone was dependent on the time of pretreatment up to 8 h. Dexamethasone had little effect on the number of vasopressin receptor and its affinity to vasopressin. The pretreatment with dexamethasone also amplified the formation of IP3 induced by NaF, a GTP-binding protein activator, or angiotensin II. 12-O-Tetradecanoylphorbol-13-acetate, a protein kinase C (PKC)-activating phorbol ester, significantly reduced the dexamethasone-induced enhancement of IP3 formation stimulated by vasopressin, angiotensin II or NaF 4 alpha-Phorbol-12, 13-didecanoate, a PKC-nonactivating phorbol ester, had little effect on the enhancement by dexamethasone. These results strongly suggest that glucocorticoid amplifies vasopressin-induced PI hydrolysis at a point downstream from GTP-binding protein in primary cultured rat aortic smooth muscle cells, and that the activation of PKC has a negative feedback effect on the amplification by glucocorticoid of vasopressin-induced PI hydrolysis.
- Published
- 1995
- Full Text
- View/download PDF
27. The expression of pituitary adenylate cyclase-activating polypeptide (PACAP) mRNA in rat brain: possible role of endogenous PACAP in vasopressin release.
- Author
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Murase T, Kondo K, Arima H, Iwasaki Y, Ito M, Miura Y, and Oiso Y
- Subjects
- Animals, Arcuate Nucleus of Hypothalamus, Autoradiography, Dehydration, In Situ Hybridization, Male, Neuropeptides physiology, Neurotransmitter Agents physiology, Pituitary Adenylate Cyclase-Activating Polypeptide, Rats, Neuropeptides genetics, Neurotransmitter Agents genetics, RNA, Messenger genetics, Vasopressins metabolism
- Abstract
We investigated the expression of pituitary adenylate cyclase-activating polypeptide (PACAP) mRNA in rat brain by in situ hybridization. PACAP mRNA was prominently expressed in arcuate nucleus (ARC). Three days of water deprivation significantly increased plasma arginine vasopressin and markedly potentiated the expression of PACAP mRNA in ARC. These results suggest that PACAP in ARC may play some physiological role, possibly one of which may be the control of vasopressin release.
- Published
- 1995
- Full Text
- View/download PDF
28. [Clinical assessment of posterior pituitary function by measurement of unextracted random urine].
- Author
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Oiso Y, Kondo K, and Otake K
- Subjects
- Adolescent, Adult, Child, Child, Preschool, Diabetes Insipidus physiopathology, Female, Humans, Infant, Male, Pituitary Function Tests methods, Pituitary Gland, Posterior physiopathology, Pregnancy, Radioimmunoassay, Random Allocation, Reference Values, Pituitary Gland, Posterior physiology, Vasopressins urine
- Abstract
To evaluate posterior pituitary function without any provocative examination, vasopressin (AVP) concentrations of random urine were measured by high-sensitive radioimmunoassay (AVP-RIA Kit, Mitsubishi Petrochemical Co., Ltd.). No apparent interference for the AVP measurement in unextracted urine was seen after appropriate dilution of urine sample. Urinary AVP did not degenerate at least for 24 hr at room temperature. AVP concentration of random urine was significantly correlated with AVP excretion in 24hr-urine in normal subjects. In 25 patients with neurogenic diabetes insipidus diagnosed by hypertonic saline infusion test, the AVP concentration in random urine was less than 13 pg/mg Cr. In approximately 1% of the normal subjects the urinary AVP level was below this range. Therefore, more intensive examinations should be planned to rule out the failure of AVP secretion in the case of such low AVP level in random urine. We also investigated the physiological changes in AVP secretion in 815 children and 352 pregnant women by measurement of urinary AVP. Even a large number of samples could be measured using this simple procedure.
- Published
- 1991
29. Osmoregulation of plasma vasopressin in myxedema.
- Author
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Iwasaki Y, Oiso Y, Yamauchi K, Takatsuki K, Kondo K, Hasegawa H, and Tomita A
- Subjects
- Adult, Aged, Female, Humans, Hypothyroidism blood, Hypothyroidism complications, Middle Aged, Myxedema diagnosis, Myxedema etiology, Osmolar Concentration, Radioimmunoassay, Thyroid Hormones blood, Thyroid Hormones deficiency, Thyrotropin blood, Water Deprivation, Water-Electrolyte Balance, Myxedema blood, Vasopressins blood
- Abstract
We studied osmoregulation of plasma vasopressin (AVP) in eight patients with untreated myxedema due to primary hypothyroidism. All patients had severe thyroid hormone deficiency due to chronic thyroiditis and had been receiving no medication at the time of this study. AVP release was defined by 5% hypertonic saline infusion test in all patients, and urinary diluting capacity was estimated by the iv water-loading tests in five patients. Plasma AVP was measured by sensitive and specific RIA. The mean basal plasma AVP level in the patients (0.5 +/- 0.1 pmol/L) was significantly lower (P less than 0.01) than that in normal adults (2.5 +/- 0.5 pmol/L). During hypertonic saline infusion, the rise in plasma AVP was normal or subnormal in all patients. In two patients who showed mild to moderate hyponatremia in the basal state and mild urinary diluting defect during water loading, plasma AVP was appropriately suppressed in each case. These results indicate that inappropriate elevation of plasma AVP is not common in myxedema, and that impaired water excretion is due mainly to AVP-independent mechanisms.
- Published
- 1990
- Full Text
- View/download PDF
30. Plasma osmolality and exocrine pancreatic secretion.
- Author
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Kitagawa M, Hayakawa T, Kondo T, Shibata T, and Oiso Y
- Subjects
- Animals, Dogs, Female, Injections, Intravenous, Islets of Langerhans drug effects, Male, Osmolar Concentration, Saline Solution, Hypertonic, Vasopressins administration & dosage, Vasopressins blood, Islets of Langerhans metabolism, Plasma physiology, Vasopressins pharmacology
- Abstract
To confirm the influence of plasma osmolality on exocrine pancreatic secretion, hypertonic saline (4% saline) was given intravenously to dogs with gastric and pancreatic fistulae. Intravenous administration of hypertonic saline caused a reduction of pancreatic juice flow and bicarbonate output, but did not alter protein output stimulated by secretin and cerulein. The changes of pancreatic juice flow(X) exhibited negative correlations with the changes in plasma osmolality(Y) (Y = -2.2X + 6.4, r = -0.74, p less than 0.01). Plasma osmolality and plasma vasopressin level were measured simultaneously. Plasma osmolality was elevated from 292 to 315 mOsm/kg with concurrent increase of plasma vasopressin level from 2.4 to 19.6 pg/mL. On the other hand, exogenous administration of vasopressin inhibited pancreatic juice flow and bicarbonate output dose-dependently. In conclusion, elevation of plasma osmolality decreased exocrine pancreatic secretion stimulated by secretin and cerulein, and vasopressin may play an important role in its mechanism.
- Published
- 1990
- Full Text
- View/download PDF
31. Diprenorphine inhibits selectively the vasopressin response to hypovolemic stimuli.
- Author
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Robertson GL, Oiso Y, Vokes TP, and Gaskill MB
- Subjects
- Animals, Hypotension physiopathology, Male, Naloxone pharmacology, Nitroprusside pharmacology, Rats, Rats, Inbred Strains, Saline Solution, Hypertonic, Diprenorphine pharmacology, Hematocrit, Morphinans pharmacology, Shock physiopathology, Vasopressins blood
- Published
- 1985
32. [Radioimmunoassay of vasopressin in unextracted random urine; clinical application for screening of central diabetes insipidus].
- Author
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Kondo K, Otake K, Iwasaki Y, Oiso Y, and Takatsuki K
- Subjects
- Diabetes Insipidus urine, Female, Humans, Male, Radioimmunoassay, Diabetes Insipidus prevention & control, Mass Screening, Vasopressins urine
- Abstract
The concentration of unextracted urinary arginine vasopressin (UAVP) was directly measured by high-sensitive radioimmunoassay (AVP-RIA Kit, Mitsubishi Petrochemical Co., Ltd.). Urine was diluted to eliminate interference of nonspecific substance without prior extraction. When urine aliquots were diluted in 4 to 32 fold in assay buffer, the relationship between UAVP concentration and dilution ratio corresponded exactly in a linear regression line. The elution pattern on Sephadex G-25 of UAVP immunoreactivity was identical with that of synthesized AVP. The AVP concentration in unextracted urine was not significantly different from that of extracted urine by Sep-Pak C18 column (Water Associates, Milford MA). The mean recovery of added AVP to urine specimens was 101.1 +/- 9.8% (mean +/- SD). The immunoreactivity of UAVP was not modified by either albuminuria (50 and 100 mg/dl) or glycosuria (1000 g/dl). Mean coefficients of variance between-assay and within-assay were 8.3% and 6.6% respectively. In normal subjects (n = 28), significant correlation was observed between UAVP concentration and simultaneously measured plasma AVP (r = 0.701, p less than 0.001). Moreover, AVP concentration in random urine was significantly correlated with AVP excretion in 24 hr-urine (r = 0.703, p less than 0.05, n = 9), and this suggested that random UAVP concentration may indicate daily UAVP secretion. In normal subjects, AVP concentration in random urine was widely scattered from 9.2 to 470.6 pg/mg Cr (89.5 +/- 76.4 pg/mg Cr, n = 211). In patients with diabetes insipidus (DI), UAVP concentration (1.6 to 13.0 pg/mg Cr, 6.94 +/- 2.77 pg/mg Cr, n = 25) was significantly lower (p less than 0.001) than that of normal subjects. UAVP concentration in a patient with primary polydipsia (43.2 pg/mg Cr) was not similar to that of ID but to that of normal subjects. UAVP concentration in 2 patients with SIADH was not more than that of normal subjects, indicating that random UAVP concentration is not suitable for detecting inappropriate AVP secretion. In this study, it is suggested that patients of random UAVP concentration below 13.0 pg/mg Cr should be recommended other intensive examination to diagnose DI, even though 2 normal subjects (0.9%) were incorrectly estimated as DI. In conclusion, radioimmunoassay of AVP in unextracted random urine is easy to sample and assay, and useful in screening polyuric patients.
- Published
- 1989
- Full Text
- View/download PDF
33. [The effects of various anaesthetics on rat vasopressin release (author's transl)].
- Author
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Oiso Y and Tomita A
- Subjects
- Animals, Carbamates pharmacology, In Vitro Techniques, Male, Osmolar Concentration, Pentobarbital pharmacology, Radioimmunoassay, Rats, Rats, Inbred Strains, Anesthetics pharmacology, Vasopressins blood
- Published
- 1981
- Full Text
- View/download PDF
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