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)

The ability of vasopressin to stimulate the accumulation of 3H-labelled inositol phosphates was studied in vitro using prelabelled rat anterior pituitary quarters. [8-Arginine] vasopressin activates inositol lipid breakdown in this system in a time- and dose-dependent manner; vasopressin (3 X 10(-7) M) resulted in a 1.8-fold stimulation of inositol phosphate accumulation over control accumulation after 10 min. This response to vasopressin is inhibited by the specific V1 antagonist (CH2)5Tyr(Me)AVP. Both oxytocin and the selective V2 agonist DDAVP also show some agonist activity, but are considerably less potent than arginine vasopressin. Corticotrophin-releasing factor alone had no effect on inositol phosphate production, whilst a high dose given in conjunction with vasopressin resulted in a diminution of the response below that found with the same concentration of vasopressin alone. Anterior pituitaries from vasopressin-deficient Brattleboro rats also show a phosphatidylinositol response to vasopressin. Pituitaries from rats that had been adrenalectomized 4 days earlier showed no increase in inositol phosphate accumulation in response to vasopressin. Daily administration of dexamethasone (40 micrograms/day) reversed this effect of adrenalectomy. This reversal was not seen when dexamethasone (40 micrograms/ml) was added to the incubation medium of adrenalectomized rat pituitary quarters. These results confirm that the rat anterior pituitary contains functional vasopressin receptors capable of activating inositol phospholipid metabolism and that this biochemical response is modified by changes in the hypothalamo-pituitary-adrenal axis.
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PMID:Vasopressin activation of phosphatidylinositol metabolism in rat anterior pituitary in vitro and its modification by changes in the hypothalamo-pituitary-adrenal axis. 356 97

We describe a 30 year old man who developed chronic adipsic hypernatraemia and hypothermia following a subarachnoid haemorrhage from an anterior communicating artery aneurysm. Anterior pituitary function tests were normal. Hypothermia was demonstrated over 4 years with loss of the ability to control heat conservation despite body temperatures as low as 30 degrees C. He failed to experience thirst despite plasma sodium concentrations of up to 187 nmol/l and plasma osmolalities of up to 397 mOsm/kg. The slope of the plasma vasopressin-plasma osmolality curve indicated loss of the osmoreceptor. There was an absent vasopressin response to insulin-induced hypoglycaemia but a normal response to apomorphine. The apomorphine-stimulated immunoreactive vasopressin was shown to behave identically to the synthetic peptide on HPLC and was bioactive.
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PMID:Chronic hypernatraemia and hypothermia following subarachnoid haemorrhage. 377 77

Tissue ir-dynorphin has been shown to be associated with three components separable by gel filtration. Similar components were found in both pituitary and brain, although there are differences in the relative amounts of each component in each tissue. Anterior lobe of rat pituitary contains predominantly the component with highest apparent molecular weight, while the component with smallest apparent molecular weight, which is the major form in neurointermediate lobe, was absent. Exposure of rats to NaCl resulted in a parallel depletion of ir-dynorphin and ir-[Arg]-vasopressin neurointermediate lobe stores. Thus a role for dynorphin, acting in concert with vasopressin, or in the regulation of vasopressin release, appears possible.
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PMID:Dynorphin immunoreactivity in pituitary. 612 5

Dynorphin is found mainly in the particulate fraction of rat pituitary gland and hypothalamus homogenates. Dynorphin-like immunoreactivity (DYN-LI) from neurointermediate lobe (NIL) homogenates migrates at the same rate as vasopressin-like immunoreactivity (AVP-LI), in sucrose density gradients, whereas DYN-LI from the hypothalamus appears to migrate principally in a less dense region of the gradient. This suggests that dynorphin and vasopressin from pituitary are present in organelles of similar size and density, while the bulk of the dynorphin in the hypothalamus appears to be stored in a different subcellular organelle. Anterior lobe (AL) dynorphin appears to migrate in two separate bands on density gradients: the less dense band (slower) migrates at a similar rate to that of dynorphin and vasopressin from NIL. When alpha-neo-endorphin was measured in sucrose gradients of NIL and hypothalamus, it was found to co-migrate with DYN-LI.
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PMID:Subcellular localization of immunoreactive dynorphin and vasopressin in rat pituitary and hypothalamus. 613 Apr 35

Median eminence corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) and pituitary and peripheral plasma adrenocorticotropin (ACTH) and AVP were measured in male Wistar rats 1 and 2 weeks after bilateral adrenalectomy (ADX), sham operation (SHAM) or dexamethasone-treatment (DEX). Median eminence AVP content was unchanged 1 week after ADX but was significantly elevated 2 weeks after ADX, whereas CRF activity was reduced at 1 week after ADX and returned to control range at 2 weeks. Anterior pituitary ACTH content was elevated but posterior pituitary AVP content was reduced at 1 and 2 weeks after ADX. Plasma ACTH was greatly elevated in ADX rats and reduced in DEX rats, whereas plasma AVP did not differ significantly between these two groups or the control group. When ADX and SHAM rats were laparotomized under ether, plasma ACTH increased greatly, but this elevation was prevented by DEX treatment. The plasma AVP level was elevated in all three groups 2.5 min after onset of stress but returned to the basal range at 20 min. Median eminence CRF and AVP and pituitary ACTH and AVP were not significantly changed after onset of stress. These results indicate that the vasopressin and CRF-ACTH responses were not consistent in the median eminence, pituitary and peripheral plasma and suggest that vasopression is not involved in the feedback and acute stress mechanism of CRF-ACTH secretion. However, we have to measure CRF activity and AVP concentration in the hypophysial portal blood to confirm this conclusion.
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PMID:Vasopressin and CRF-ACTH in adrenalectomized and dexamethasone-treated rats. 625 47

We measured [3H]prolactin ([3H]Prl) synthesis and secretion in female rat anterior hemipituitary glands incubated in vitro, and immunoassayable Prl secretion from dispersed anterior pituitary cells in a perfused column. Anterior pituitary glands which were incubated in 9 microM reserpine showed a marked inhibition of [3H]Prl secretion but no change in hormone synthesis, thus causing [3H]Prl accumulation within the gland. The same concentration of reserpine produced a similar effect in pituitary glands taken from rats depleted of dopamine with alpha-methyl-p-tyrosine. Reserpine inhibited Prl secretion from dispersed anterior pituitary cells with a gradual onset and prolonged duration. Thyrotropin-releasing hormone (TRH), but not dibutyryl cyclic AMP (dbcAMP), the calcium ionophore A23187 or excess Ca2+, stimulated both [3H]Prl and Prl secretion in the presence of reserpine. In contrast, neither basal nor vasopressin-stimulated ACTH (bio- and immunoassayable) secretion was inhibited by 9 microM reserpine. Ultrastructurally, pituitary glands incubated in reserpine had an increased content of Prl secretory granules. Reserpine thus selectively inhibited Prl secretion, secondarily causing accumulation of both measurable hormone and Prl secretory granules within the pituitary gland. We hypothesize that reserpine interrupted calcium-dependent mechanisms in the stimulus-secretion coupling process to inhibit Prl release.
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PMID:Reserpine inhibits rat anterior pituitary hormone secretion in vitro: effects on prolactin and ACTH and ultrastructural observations. 629 87

Fragments of adrenocorticotropic hormone (ACTH) cell adenomas and anterior lobes of two patients with Cushing's disease were obtained by transnasal operation. Both patients showed the typical clinical course, with postoperative ACTH deficit and all other pituitary functions intact. Equivalent specimens of tissue were investigated by immunocytology and in a superfusion system. The majority of adenoma cells were ACTH-positive, whereas ACTH-secreting cells of the anterior lobes were mostly inactive and were reduced in number. In vitro, adenomatous tissue showed high ACTH secretion into the superfusion medium, which was increased significantly after vasopressin application. Corticoid feedback was impaired Anterior lobe cells exhibited a significant spontaneous ACTH secretion that was reduced by cortisol, but not stimulated by vasopressin. These results support the concept of an impaired corticoid feedback at the adenoma level in the presence of suppressed ACTH secretion of the para-adenomatous anterior lobe.
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PMID:In vitro secretion of adenoma and anterior lobe cells in two typical cases of Cushing's disease. 630 1

In pathological or experimental hyperprolactinemia, the elevated circulating levels of PRL are the usual cause of the impairment in gonadotropic function. The present study was undertaken to determine whether PRL could suppress basal LH secretion and LHRH-stimulated LH release by a direct action at the anterior pituitary. Anterior pituitaries from ovariectomized rats were incubated in medium 199 alone or in medium 199 containing ovine PRL, and basal and the LHRH-stimulated LH release were followed for 2 or 3 h in vitro. Ovine PRL at 40 and 80 micrograms/ml suppressed basal LH release by 41% and 72%, respectively, at 2 h of incubation. This suppressive effect of both concentrations of PRL continued to the third hour of incubation. LHRH at 5 ng/ml increased the release of LH from pituitaries incubated in medium alone by 57%, 61%, and 107% at 1, 2, and 3 h of incubation, respectively. However, in the pituitaries treated with 40 micrograms/ml ovine PRL, the stimulatory effects of LHRH were diminished at all time points measured. Pretreatment of anterior pituitaries with ovine PRL for 6 h significantly inhibited by 81% the LHRH (5 ng/ml) stimulation of LH release at 2 h of incubation. On the other hand, inhibition of endogenous PRL release by 10(-6) M bromocriptine enhanced the stimulatory effects of 5 ng/ml LHRH by 2.5-fold at 2 h of incubation. The inhibitory effects of PRL on basal and stimulated LH secretion appeared unique, since neither BSA nor vasopressin could elicit similar suppressive effects on LH. These results suggest that in anterior pituitaries exposed to elevated levels of PRL, LH secretion and pituitary responsiveness to LHRH could be impaired. This phenomenon may contribute in part to the antigonadotropic effects of PRL.
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PMID:Prolactin suppresses luteinizing hormone secretion and pituitary responsiveness to luteinizing hormone-releasing hormone by a direct action at the anterior pituitary. 634 62

We have previously characterized specific oxytocin receptors in the rat anterior pituitary gland, using a highly selective oxytocin receptor antagonist as radioligand. The aim of the present study was to examine whether occupation of these receptors by oxytocin produces a stimulation of prolactin release and a rise in the accumulation of total inositol phosphates in the rat adenohypophysis. Anterior pituitary cells harvested from randomly cycling and diethylstilboestrol (100 micrograms s.c.)-treated rats were perifused with Dulbecco's minimal essential medium at a rate of 0.3 ml/min. Oxytocin and the specific oxytocin agonist [Thr4-Gly7]-oxytocin (TG-OT) both stimulated a significant prolactin release at concentrations of 10(-6) and 10(-7) M. Oestrogen treatment did not affect the response to oxytocin, indicating that there is no straightforward correlation between receptor number and prolactin secretory response in the rat pituitary gland. The involvement of phosphoinositide hydrolysis was investigated in dispersed anterior pituitary cells and uterine tissue from randomly cycling rats. Oxytocin and arginine-vasopressin stimulated a significant (P < 0.05) and dose-related increase in total inositol phosphates, vasopressin being more potent. The specific oxytocin agonist TG-OT had no effect on total inositol phosphate production in pituitary cells, but when tested in uterine tissue it significantly (P < 0.05) stimulated the accumulation of total inositol phosphate at all concentrations tested (10(-5) to 10(-9) M). In conclusion, the data show that oxytocin has prolactin-releasing activity, acting on specific receptors in the anterior pituitary gland.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Specific oxytocin agonist stimulates prolactin release but has no effect on inositol phosphate accumulation in isolated rat anterior pituitary cells. 838 9

Pituitary function was assessed in healthy adult beagle dogs before and after hypophysectomy. Anterior pituitary function was tested by use of the combined anterior pituitary (CAP) function test, which consisted of sequential 30-sec intravenous injections of four hypothalamic releasing hormones, in the following order and doses: 1 microgram of corticotropin-releasing hormone (CRH)/kg, 1 microgram of growth hormone-releasing hormone (GHRH)/kg, 10 micrograms of gonadotropin-releasing hormone (GnRH)/kg, and 10 micrograms of thyrotropin-releasing hormone (TRH)/kg. Plasma samples were assayed for adrenocorticotropin (ACTH), cortisol, GH, luteinizing hormone (LH), and prolactin (PRL) at multiple times for 120 min after injection. Pars intermedia function was assessed by the alpha-melanotropin (alpha-MSH) response to the intravenous injection of the dopamine antagonist haloperidol in a dosage of 0.2 mg/kg. Posterior pituitary function was assessed by the plasma vasopressin (AVP) response to the intravenous infusion of 20% saline. Basal plasma ACTH, cortisol, thyroxine, LH. PRL, and AVP concentrations were significantly lower at 10 wk after hypophysectomy than before hypophysectomy. In the CAP test and the haloperidol test, the peaks for the plasma concentrations of ACTH, cortisol, GH, LH, PRL, and alpha-MSH occurred within 45 min after injection. At 2 and 10 wk after hypophysectomy, there were no responses of plasma GH, LH, PRL, and alpha-MSH to stimulation. In four of eight hypophysectomized dogs, there were also no plasma ACTH and cortisol responses, whereas in the other four dogs, plasma ACTH and cortisol responses were significantly attenuated. The basal plasma ACTH and cortisol concentrations were significantly lower in the corticotropic nonresponders than in the responders. Plasma AVP responses were completely abolished by hypophysectomy, although water intake by the dogs was normal. Histopathological examinations at 10 wk after hypophysectomy revealed that adrenocortical atrophy was much more pronounced in the corticotropic nonresponders than in the responders. No residual pituitary tissue was found along the ventral hypothalamic diencephalon. However, in all hypophysectomized dogs that were investigated, islets of pituitary cells were found embedded in fibrous tissue in the sella turcica. A significant positive correlation was found between the number of ACTH-immunopositive cells and the ACTH increment in the CAP test at 10 wk after hypophysectomy. It is concluded that 1) stimulation of the anterior pituitary with multiple hypophysiotropic hormones, stimulation of the pars intermedia with a dopamine antagonist, and stimulation of the neurohypophysis with hypertonic saline do not cause side effects that would prohibit routine use, 2) in the routine stimulation of the anterior pituitary and the pars intermedia, blood sampling can be confined to the first 45 min, 3) the ACTH and cortisol responses to hypophysiotropic stimulation are the most sensitive indicators for residual pituitary function after hypophysectomy, 4) small islets of pituitary cells in the sella turcica, containing corticotropic cells, are the most likely source of the attenuated corticotropic response that may occur after hypophysectomy, and 5) residual AVP release from the hypothalamus after hypophysectomy is sufficient to prevent diabetes insipidus, despite the fact that the AVP response to hypertonic saline infusion is completely abolished.
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PMID:Assessment of pituitary function after transsphenoidal hypophysectomy in beagle dogs. 906 51


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