UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies involving fluid homeostasis were carried out in adult Long-Evans rats born to mothers given liquid diets containing 35% of the calories derived from ethanol and compared to offspring of dams given isocaloric liquid diets containing no ethanol. Plasma levels of arginine vasopressin (AVP), plasma and urine osmolality, and urine production were determined in water-sated and water-deprived offspring. In the water-sated condition, the group exposed to alcohol prenatally had plasma levels of AVP seven-fold above control levels. This increase was associated with a large increase in within-group variability. Water consumption was also significantly elevated in the group of fetal alcohol exposed (FAE) rats. Plasma and urine osmolality and urine production were similar to control levels. In the control animals, 24-hr of water deprivation produced the expected increase in AVP, in plasma and urine osmolality, and decrease in urine production. The FAE animals, however, showed parallel changes in plasma and urine osmolality and urine production with no significant change in AVP. Examination of basal glucose metabolic rates in the cerebral structures involved in fluid homeostasis revealed that despite the large increase in AVP levels in the FAE rats, only the neurohypophysis and supraoptic nuclei showed significant increases in activity. These data suggest that fetal alcohol exposure causes a long-term disruption in the central mechanisms regulating vasopressin release and fluid homeostatic responses.
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PMID:Arginine vasopressin and body fluid homeostasis in the fetal alcohol exposed rat. 273 78

1. The cardiovascular effects of pressor doses of arginine vasopressin were examined in anaesthetized Brattleboro rats with hereditary diabetes insipidus (BDI) and normal rats of the parent Long Evans (LE) strain, either 37 or 85 days old. 2. Control mean arterial blood pressure and total peripheral resistance were similar in adult animals of the two strains but were significantly lower in the young BDI rats compared with the young LE rats. 3. The three doses of vasopressin produced greater pressor responses in the young, immature LE rats compared with the young BDI rats, whereas in the adult animals vasopressin had the greater pressor effect in the BDI rats compared with the LE rats of comparable age. 4. There was little effect of vasopressin on cardiac output after the initial decrease, particularly in the BDI rats whether immature or adult, despite more prolonged decreases in heart rate. 5. These studies indicate important age-related differences in the pressor response to vasopressin in anaesthetized rats, in addition to the clear differences in response between the animals with (LE) or without (BDI) the circulating endogenous peptide.
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PMID:Haemodynamic responses to vasopressin in anaesthetized young and adult Brattleboro rats. 273 85

The cardiovascular effects of centrally administered cholinomimetics were examined in conscious Long-Evans and Brattleboro rats. Carbachol (1 microgram/kg) or physostigmine (50 micrograms/kg) induced a long-lasting increase in blood pressure and a decrease in heart rate in Long-Evans rats whereas no bradycardia was observed in Brattleboro rats, and the pressor response was significantly less than that in Long-Evans rats. The cardiovascular responses to nicotine (30 micrograms/kg) in Brattleboro rats were not different from those in Long-Evans rats. Intravenous vasopressin antagonist, d(CH2)5Tyr(Me) arginine vasopressin, significantly attenuated the pressor response and eliminated the bradycardic response to carbachol in Long-Evans rats. However, the pressor response to carbachol in Brattleboro rats was still significantly less than that in Long-Evans rats treated with vasopressin antagonist. Intravenous phentolamine partially inhibited the pressor response to carbachol in Long-Evans rats and completely eliminated it in Brattleboro rats. Combined intravenous treatment with phentolamine and vasopressin antagonist completely eliminated the pressor response to carbachol in Long-Evans rats. Centrally administered methylatropine eliminated either the hypertensive or bradycardic response to carbachol in Long-Evans rats. These results indicate that the pressor and bradycardic response to carbachol or physostigmine is mediated by the central muscarinic receptor mechanism. Hypertensive response to intracerebroventricularly administered carbachol in normal rats is mediated both by an increase in central sympathetic outflow and in circulating vasopressin. The bradycardia seems to be mediated mainly by vasopressin.
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PMID:Role of vasopressin in cardiovascular response to central cholinergic stimulation in rats. 273 6

Acetylcholinesterase activity was demonstrated histochemically at light- and electron-microscopic levels, in Vibratome sections of the supraoptic nucleus of fixed hypothalami derived from osmotically stimulated and unstimulated Long Evans rats, from homozygous Brattleboro rats with hypothalamic diabetes insipidus, from lactating rats, from normal adult male house mice (Mus musculus) and from mice with hereditary nephrogenic diabetes insipidus (di/di). Reaction product was located in supraoptic magnocellular neurons; in dorsal and rostral aspects of the supraoptic nuclei lightly stained cells predominate, whereas in ventral and caudal regions densely staining perikarya predominate. Pre- and post-embedding immunocytochemical detection of oxytocin-neurophysin or vasopressin-neurophysin, combined with acetylcholinesterase histochemistry, showed that the lightly staining cells are oxytocinergic, and the densely staining cells vasopressinergic. Osmotic stimulation of the animals, either by substitution of drinking water for 3 days with 2.5% saline or reason of genetic defects which result in diabetes insipidus, enhanced the acetylcholinesterase activity of the vasopressin neurons but had little effect on the weekly acetylcholinesterase-reactive oxytocin cells. Acetylcholinesterase activity was particularly marked in the hypertrophied abnormal magnocellular neurons of homozygous Brattleboro rats which do not release significant amounts of vasopressin. The increased acetylcholinesterase activity in osmotically stimulated animals cannot, therefore, be a function of vasopressin. Acetylcholinesterase activity was also detected in large multipolar neurons lying dorsolateral to the supraoptic nucleus, and in their fine axonal processes which project towards the supraoptic nucleus. A very few synaptic boutons surrounded by acetylcholinesterase reaction product were found in contact with magnocellular neuron basal dendrites. However, much of the punctate acetylcholinesterase reactivity observed at the light microscopic level and previously interpreted as representing the loci of cholinergic synaptic boutons was shown to be intracellular, and probably caused by acetylcholinesterase activity in some large, secondary lysosomes.
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PMID:Differential distribution of acetylcholinesterase activity among vasopressin- and oxytocin-containing supraoptic magnocellular neurons. 276 86

Fetal tissues obtained from specific regions of the developing hypothalamus were transplanted to determine whether the precursor neurons of the suprachiasmatic nucleus (SCN) can be distinguished from those of the presumptive paraventricular nucleus (PVN) on the basis of the functional capacity to generate circadian rhythms. The presumptive SCN, the PVN, and a portion of the neocortical primordium were dissected from the developing forebrains of normal Long-Evans fetuses, separated, and selectively transplanted into the periventricular-third ventricle region of adult, vasopressin (VP)-deficient Brattleboro rats. In host animals that received grafts containing the precursor population of SCN neurons, the temporal profile of VP levels in the cerebrospinal fluid (CSF) oscillated with a circadian periodicity in a manner similar to that observed in normal Long-Evans rats. CSF collected serially from animals with grafts of the presumptive PVN also contained VP, but no circadian variation was manifested in peptide levels. VP was undetectable in CSF samples obtained from Brattleboro rats with cortical grafts. In association with their circadian functional capacity, grafts of the SCN primordium were characterized by clusters of parvicellular neurons immunopositive for VP or vasoactive intestinal polypeptide (VIP) that resembled the cell groups of the in situ SCN. In contrast, transplants of the presumptive PVN did not contain neurons immunoreactive for VIP, and the VP neurons in these grafts resembled the neurosecretory cells of the PVN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Specificity of circadian function in transplants of the fetal suprachiasmatic nucleus. 276 62

The role of vasopressin (VP) in the regulation of pituitary corticotropin-releasing factor (CRF) receptors was studied by examining the effects of adrenalectomy and VP infusion on pituitary CRF receptors in genetically VP-deficient rats (di/di) and Long-Evans control rats. Binding studies with [125I]Tyr-ovine CRF in 30,000 X g anterior pituitary membrane-rich fractions revealed similar characteristics for the CRF receptors in Long-Evans and di/di rats, with Kd values of 2.4 +/- 0.6 and 1.9 +/- 0.2 nM, respectively, and receptor concentrations of 278 +/- 31 and 286 +/- 43 fmol/mg, respectively. Two days after adrenalectomy, the pituitary CRF receptor concentration decreased by 72 +/- 4.2% in Long-Evans rats, but by only 20.3 +/- 5.6% in di/di rats. CRF receptor affinity was unchanged after adrenalectomy (Kd = 1.7 +/- 0.5 nM; n = 8). To determine whether VP deficiency is responsible for the smaller decrease in CRF receptor in di/di rats, the effect of exogenous VP infusion (100 ng/min) by sc osmotic minipumps was studied in adrenalectomized di/di rats. Two days after adrenalectomy, pituitary CRF receptors were reduced by 21 +/- 8% in control di/di rats, whereas a 77.7 +/- 1.8% decrease was observed in VP-infused di/di rats, comparable to the effect of adrenalectomy in Long-Evans rats. VP infusion also caused a significant 35 +/- 2% decrease in CRF receptors in the pituitaries of sham-operated di/di rats, with no change in CRF receptor affinity. In Sprague-Dawley rats, VP or CRF infusion (100 ng/min) decreased pituitary CRF receptors by 14 +/- 1.9% and 46 +/- 3%, respectively. However, the combined infusion of both peptides caused a 65% +/- 4.2 decrease, similar to that observed after adrenalectomy. In vitro incubation of quartered pituitaries with VP or CRF for 4 h reduced CRF receptors by 23.1 +/- 8.2% and 38.2 +/- 3.8%, respectively, while simultaneous preincubation with both peptides was followed by a decrease of 55.3 +/- 5.3%. These findings indicate that increased hypothalamic release of VP contributes to the down-regulation of pituitary CRF receptors after adrenalectomy.
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PMID:Involvement of vasopressin in the down-regulation of pituitary corticotropin-releasing factor receptors after adrenalectomy. 282 80

L-3H-fucose was injected into the lateral cerebral ventricle of vasopressin-deficient Brattleboro and control Long-Evans rats which were subsequently killed at several time intervals after the injection. The hypothalamus and the neurohypophysis were processed for light- and electronmicroscopic radioautography. Other complementary experiments using immunocytochemical and enzyme-histochemical techniques were also undertaken. L-3H-fucose was incorporated into newly synthesized glycoproteins in the Golgi apparatus of supraoptic and paraventricular neurons, and later on labelled glycoproteins migrated to lysosomes and the plasma membrane surrounding the perikaryon. The Golgi apparatus of the vasopressin-deficient neurons remained heavily labelled as long as 3 days after injection, in sharp contrast with the normal neurons in which there was a remarkable decrease of label in the Golgi region between 4 and 24 h after the isotope administration. Labelled glycoproteins also migrated to the neurohypophysis and were mainly found in the axonal plasma membrane, vesicles and axoplasm. The renewal of glycoproteins in the neurohypophysis of Brattleboro rats was faster than in the normal rats and this was attributed to the lack of formation of products which are normally packaged in secretory granules in the perikaryon and released at the axon terminal in the neurohypophysis. Colchicine caused a disturbance in the topography of the organelles of the perikaryon and the most striking features were the displacement of Golgi stacks to the periphery of the perikaryon and an accumulation of mitochondria in this neuronal region. No secretory granules were observed in the vasopressin-deficient neurons of untreated or colchicine-treated Brattleboro rats. By contrast, secretory granules (most of them labelled with 3H-fucose) were concentrated in the perikaryon of colchicine-treated Long-Evans rats. In these rats, colchicine caused a severe block in the migration of 3H-fucose-labelled glycoproteins to the neurohypophysis, but this did not occur in the Brattleboro rats. The results of the experiments were interpreted in the light of the genetic defect known to occur in Brattleboro rats which causes the inability to produce vasopressin and also remarkable morphological and physiological changes in the affected neurons.
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PMID:Radioautographic study of glycoprotein synthesis and fate in the hypothalamo-neurohypophyseal system of vasopressin-deficient Brattleboro rats. 282 60

Oxytocin and vasopressin binding sites were localized and characterized by quantitative autoradiography on consecutive sections of Long-Evans rat forebrains and pituitary glands, incubated in the presence of 5 nM [3H]oxytocin or 5 nM [3H]vasopressin. In the forebrain, two types of neurohypophysial hormone binding sites were thus defined. (1) Oxytocin/vasopressin sites with similar nanomolar-range affinities for [3H]oxytocin and [3H]vasopressin; both tritiated peptides were displaced from these sites in the presence of 10 microM of either oxytocin or vasopressin. The main areas bearing such sites were the ventral subiculum, several nuclei of the amygdala, the ventromedial hypothalamic nucleus, the bed nucleus of the stria terminalis and the olfactory tubercle. (2) Selective vasopressin sites, binding [3H]vasopressin with nanomolar-range affinity and [3H]oxytocin with a much lower affinity; these sites were not labelled in the presence of 5 nM [3H]oxytocin, and 10 microM oxytocin displaced [3H]vasopressin binding by 80%. Such sites occurred in several thalamic nuclei, in the dopaminergic A13 cell group of the zona incerta, the suprachiasmatic nucleus, the fundus striati and the lateral septal nucleus. No selective oxytocin sites were detected. Different oxytocin and vasopressin binding characteristics were found in the hypothalamo-neurohypophysial system. In the paraventricular and supraoptic nuclei and in the pituitary neural lobe the [3H]vasopressin binding density was twice that of [3H]oxytocin; vasopressin was always more potent than oxytocin in displacing both [3H]vasopressin and [3H]oxytocin binding from those sites. Interaction of the tritiated peptides with neurophysins cannot be completely ruled out in these locations. The present data are discussed in correlation with the functional roles of the neurohypophysial peptides in the brain and the pharmacological characteristics of their receptors.
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PMID:Quantitative autoradiographic mapping of neurohypophysial hormone binding sites in the rat forebrain and pituitary gland--I. Characterization of different types of binding sites and their distribution in the Long-Evans strain. 284 90

The anatomical distribution and pharmacological characteristics of the different types of neurohypophysial hormone binding sites were compared in the forebrains and pituitary glands of Long-Evans rats and its mutant Brattleboro strain, genetically deficient in vasopressin. Quantitative autoradiography on sections incubated in the presence of 5 nM of either [3H]oxytocin or [3H]vasopressin revealed the presence of the same types of sites in the brains of both strains but noticeable variations in their densities were found in several areas. In the forebrain, oxytocin/vasopressin sites, which bind both peptides with similar high nanomolar affinities, had the same locations and densities in the ventral subiculum, in several nuclei of the amygdala, the bed nucleus of the stria terminalis and the olfactory tubercle. The density of such sites was, in contrast, lower in the ventromedial hypothalamic nucleus of the Brattleboro rat. Selective vasopressin sites which bind [3H]vasopressin with a nanomolar-range affinity and [3H]oxytocin with a much lower affinity showed more variations. They were not found in the Brattleboro rat thalamus but were highly concentrated in several thalamic nuclei in the Long-Evans rat. Conversely, their densities were higher in the dopaminergic A13 cell group of the zona incerta and the suprachiasmatic nucleus of the Brattleboro rat. Their densities were similar in the lateral septal nucleus and in the fundus striati of both strains. In the hypothalamo-neurohypophysial system, [3H]oxytocin and [3H]vasopressin binding occurred in the Long-Evans rat with characteristics different from those found in other brain areas. In the Brattleboro rat, no [3H]vasopressin binding and only low [3H]oxytocin binding, restricted to the magnocellular nuclei, were found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative autoradiographic mapping of neurohypophysial hormone binding sites in the rat forebrain and pituitary gland--II. Comparative study on the Long-Evans and Brattleboro strains. 284 91

To determine the interaction between alpha 1-adrenergic and vasopressinergic mechanisms in the central regulation of cardiovascular functions, the effects of intracerebroventricular (i.c.v.) administration of the alpha 1-agonists, methoxamine and phenylephrine, were examined in conscious Long-Evans (LE) rats and Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI). In LE rats, i.c.v. methoxamine and phenylephrine (3-30 micrograms/kg) increased blood pressure and decreased heart rate in a dose-related manner, while they had no detectable cardiovascular effects in DI rats. Neither i.c.v. (0.5 ng/kg per min, 1 h) nor intravenous (i.v., 2 ng/kg per min, 2 h) infusion of vasopressin (AVP) restored the cardiovascular response to i.c.v. phenylephrine in DI rats. In LE rats, however, i.v. pretreatment with the specific antagonist to the pressor effect of AVP, d(CH2)5Tyr(Me)AVP (10 micrograms/kg), attenuated the hypertensive and bradycardic effects of i.c.v. phenylephrine, while i.c.v. pretreatment with AVP antagonist (300 ng/kg) did not alter the cardiovascular response to i.c.v. alpha 1-agonist. The cardiovascular response to i.c.v. phenylephrine was blocked by i.c.v. pretreatment with the alpha 1-antagonist, prazosin (2 micrograms/kg). Intracerebroventricular phenylephrine increased plasma AVP levels 14-fold without affecting plasma angiotensin II levels. The present study clearly demonstrated that endogenous AVP plays a significant role in the cardiovascular response to i.c.v. alpha 1-agonist.
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PMID:Importance of endogenous vasopressin in the hypertensive and bradycardic response to central alpha 1-adrenergic stimulation. 286 22

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