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

Several lines of evidence have suggested that neurohypophysial vasopressin secretion is under the influence of glucocorticoid negative feedback. Studies in clinical and experimental adrenal insufficiency have suggested that the impaired water excretion accompanying that syndrome may be due to elevated vasopressin levels. Furthermore, both the impaired water excretion and elevated vasopressin levels observed in adrenal insufficiency may be normalized by glucocorticoid treatment. This topic remains controversial, with a considerable body of evidence suggesting that vasopressin is elevated during adrenal insufficiency not because of a loss of central steroid negative feedback but because of alterations in plasma volume osmolality (renal mechanisms). Vasopressin responses to a variety of stimuli (hemorrhage, hypoxia, hypertonic saline) in normal humans and animals appear to be attenuated or eliminated by pretreatment with glucocorticoids. However, the vasopressinergic system appears to be considerably less sensitive to negative feedback than the corticotropin-releasing factor-adrenocorticotropic hormone (ACTH) system. There is evidence that the locus for this inhibitory effect is both directly at the posterior pituitary and within the hypothalamus. It is unlikely that corticosteroid negative feedback closes a direct hypothalamo-neurohypophysial-adrenocortical feedback loop. Since neurohypophysial vasopressin is involved in the control of ACTH secretion, it is more likely that the modulation of neurohypophysial vasopressin by glucocorticoid is an integral part of the overall negative-feedback control of ACTH secretion. The physiological role of glucocorticoid inhibition of vasopressin secretion remains speculative.
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PMID:Glucocorticoid inhibition of neurohypophysial vasopressin secretion. 303 1

Optic nerve hypoplasia is a developmental anomaly of the retina and optic nerves in which there is a reduction in the number of ganglion cells in the retina and of their centripetal fibers projecting through the optic nerve to the lateral geniculate body. The condition may be unilateral or bilateral and is frequently misdiagnosed as optic atrophy. In about 25% of cases, bilateral optic nerve hypoplasia is associated with a variety of cerebral malformations of which the commonest single disturbance is absence of the septum pellucidum (septo-optic dysplasia). Cerebral malformations and their endocrine accompaniments are also seen, though less frequently, in unilateral hypoplasia. The endocrine disturbances that may accompany optic nerve hypoplasia include growth hormone deficiency, adrenal insufficiency, hypothyroidism, and disturbances of antidiuretic hormone production. Precocious puberty and hypogonadism have also been observed. The prognosis of optic nerve hypoplasia depends upon the severity of the changes in the optic nerves and especially the degree of associated cerebral malformation. The finding of optic nerve hypoplasia should lead to thorough ophthalmologic, neurologic, and endocrinologic evaluation of the patient.
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PMID:Optic nerve hypoplasia: a review. 329 97

Corticotropin-releasing factor (CRF), a 41 amino acid polypeptide, has been isolated from ovine hypothalamic extracts, sequenced, and synthesized. It has a high potency for stimulating the secretion of corticotropin-like and beta-endorphin-like immunoactive substances in vitro and in vivo in laboratory animals and humans. The high concentration of CRF-like immunoactivity in hypophyseal portal plasma supports the hypothesis that CRF is the physiological hypothalamic factor. Human and rat CRF (rCRF) also have been purified and synthesized. They have an 83% sequence homology with ovine CRF (oCRF). oCRF-like activity has been found in human hypothalamus, pituitary stalk, posterior pituitary, thalamus, cerebral cortex, cerebellum, pons, medulla oblongata, spinal cord and in the adrenal, lung, liver, stomach, duodenum and pancreas. oCRF-like activity also has been found in the human placenta and in tissues producing ectopic ACTH. The action of CRF can be potentiated by vasopressin, oxytocin, epinephrine, norepinephrine, VIP, and angiotensin II. Intracerebroventricular administration of CRF in the rat produces prolonged elevations of plasma epinephrine, norepinephrine, glucose and glucagon; elevates mean arterial pressure and heart rate; increases motor activity and exploration in familiar surroundings and oxygen consumption; and decreases feeding and sexual behavior. Testing with CRF has enabled the separation of patients with hypothalamic and pituitary adrenal insufficiency. The CRF stimulation test has been useful in distinguishing pituitary from ectopic causes of Cushing's disease. The distribution of CRF within and beyond the hypothalamus provides an anatomical context for the observation that CRF can simultaneously activate and coordinate metabolic, circulatory and behavioral responses that are adaptative in 'stressful' situations. CRF not only stimulates the pituitary-adrenal axis in man, but it also influences several aspects of CNS function which may be of relevance to psychiatric illnesses.
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PMID:Corticotropin-releasing factor (CRF)--a review. 353 10

Techniques are described in detail for a radioimmunoassay of plasma adrenocorticotropin (ACTH) that is capable of detecting hormone in unextracted normal human plasma at 1:5 dilution under the conditions described. The sensitivity of the assay is at the level of 1 mumug/ml (equivalent to 0.014 mU/100 ml). In normal subjects ACTH concentrations averaged 22 mumug/ml (equivalent to 0.308 mU/100 ml) plasma at 8-10 a.m. In a smaller group the concentrations averaged 9.6 mumug/ml (equivalent to 0.134 mU/100 ml) at 10-11 p.m. Although a circadian rhythm in normal subjects was not always well marked throughout the daytime hours, plasma ACTH usually fell to its lowest value in the late evening. In hospital patients who were not acutely ill, concentrations were infrequently above 100 mumug/ml in the morning and usually fell to significantly lower levels in the late evening. Severely ill hospital patients occasionally exhibited a.m. concentrations above 200 mumug/ml. In a group of subjects showing frequent spiking of plasma 17-OHCS concentrations throughout the day parallel spiking of plasma ACTH as well was generally observed.Metyrapone produced marked increases in plasma ACTH within 24 hr in all cases and generally within 3-6 hr except when started late in the day. Dexamethasone brought about a persistent reduction in plasma ACTH in a patient under continued treatment with metyrapone.Hypoglycemia, electroshock, surgery under general anesthesia, histalog and vasopressin administration were usually followed by significant increases in plasma ACTH concentration. Prior administration of dexamethasone blocked the response to hypoglycemia. Marked elevations in plasma ACTH were observed in patients with adrenal insufficiency off steroid therapy, in Cushing's disease after adrenalectomy even in the presence of persistent hypercortisolemia, and in some untreated patients with Cushing's disease. Umbilical cord blood contained higher plasma ACTH concentrations than maternal blood at delivery in seven of eight cases. After suppression of ACTH secretion by dexamethasone or cortisol. ACTH disappeared from plasma with half-times ranging from 22 min to 30 min in three cases studied.
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PMID:Radioimmunoassay of ACTH in plasma. 430 80

In order to determine whether or not antidiuretic hormone (ADH) is essential to the inhibition of an acute water diuresis in adrenal insufficiency, the response to oral water loads was tested in rats with hereditary hypothalamic diabetes insipidus (DI) which lack ADH. It was found that 60 min after water loads of 3 or 5% of body weight urine flow was significantly lower and urine osmolality significantly higher in adrenalectomized DI rats than in the same DI rats before removal of their adrenal glands. The efficacy of gluco- and mineralocorticoids in reversing the inhibition was then determined in the same adrenalectomized DI rats. Prednisolone alone, administered either acutely or chronically, restored the response in urine flow to that seen in the same rats before adrenalectomy, but failed to correct the defect in urinary dilution. Aldosterone when given alone tended to correct the diluting ability but not the response in urine flow. When these two adrenal cortical hormones were given simultaneously, both the urine flow and urine osmolality were nearly identical to what they had been in the same DI rats before adrenalectomy. These studies strongly suggest (a) that ADH is not essential to the inhibition of an acute water diuresis in adrenal insufficiency, although it may abet the inhibition in individuals without diabetes insipidus, which can elaborate ADH; and (b) that both gluco- and mineralocorticoids are required in adrenal insufficiency in order to fully restore the water diuresis as judged by the dual criteria of urine flow and urine osmolality.
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PMID:On the role of antidiuretic hormone in the inhibition of acute water diuresis in adrenal insufficiency and the effects of gluco- and mineralocorticoids in reversing the inhibition. 544 9

Mineralo- and glucocorticoid-deficient states, such as Addison's disease, are partly characterized by an inability to generate a maximally concentrated urine. The purpose of the present study was to develop a model of adrenal insufficiency and to determine whether changes in the intrinsic function of the collecting duct could partly account for this concentrating defect. Two kinds of experiments were performed: an assessment of the in vivo ability of adrenal-ectomized rabbits to concentrate their urine, and an examination of the intrinsic hydroosmotic responsiveness of in vitro perfused collecting ducts isolated from normal and adrenalectomized rabbits. The present study demonstrates that adrenalectomized rabbits are unable to concentrate their urine maximally, and that the in vivo administration of either deoxycorticosterone, 250 mug/kg, or dexamethasone, 50 mug/kg, restored to or toward normal their concentrating ability. When cortical collecting tubules from adrenalectomized rabbits were perfused in vitro, they demonstrated a markedly blunted hydroosmotic response to antidiuretic hormone (ADH), which was corrected by the in vitro addition of either aldosterone (50 pM) or dexamethasone (50 pM), but not progesterone (50 pM). The steroids by themselves, in the absence of ADH, had no intrinsic effect on the water permeability of the collecting duct. The blunted hydroosmotic response across cortical collecting tubules from adrenal-ectomized rabbits was corrected by the addition of either 8-bromo cyclic AMP or a potent phosphodiesterase inhibitor, 1-methyl-3-isobutylxanthine. The present studies show that the cortical collecting tubules obtained from adrenalectomized rabbits do not respond normally to ADH. The poor hydroosmotic response to ADH was corrected by exogenous aldosterone, dexamethasone, an analog of cyclic AMP, or a phosphodiesterase inhibitor. In conclusion, the present studies are consistent with the view that the concentrating defect seen in adrenal insufficiency is at least partly the result of the absence of the permissive effect that adrenal steroids exert on the ADH-induced reabsorption of water across the collecting duct. The absence of adrenal steroids results in a diminished rate of cyclic AMP accumulation in the cells of the collecting duct, either as a result of an augmented activity of cyclic AMP phosphodiesterase or a diminished rate of cyclic AMP generation.
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PMID:Urinary concentrating defect of adrenal insufficiency. Permissive role of adrenal steroids on the hydroosmotic response across the rabbit cortical collecting tubule. 615 51

In a 20-year-old woman, a complicated full-term delivery was followed by a 14-month history of galactorrhea, amenorrhea, and symptoms of hypocortisolism. Evaluation revealed the presence of an empty sella, hyperprolactinemia, and an isolated pituitary deficiency of ACTH, resulting in secondary adrenal insufficiency. The defect in ACTH secretion was apparently due to intrinsic pituitary rather than hypothalamic disease, because administration of lysine vasopressin did not stimulate ACTH release. An empty sella with hyperprolactinemia has been described before. However, to the authors' knowledge, isolated ACTH deficiency as a complication of postpartum hypopituitarism (atypical Sheehan's syndrome) in association with an empty sella and hyperprolactinemia has not previously been reported.
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PMID:Primary empty sella, hyperprolactinemia, and isolated ACTH deficiency after postpartum hemorrhage. 630 Dec 77

Among other defects in water metabolism, adrenal insufficiency is associated with an inability to concentrate urine maximally in both man and experimental animals. Recent studies in the rabbit cortical collecting tubule have suggested indirectly that this defect may result from impaired cyclic AMP (cAMP) formation in response to antidiuretic hormone stimulation. In the present study, we examined key elements of arginine vasopressin (AVP)-dependent cAMP metabolism in the papillary collecting duct (PCD), microdissected from 8-d adrenalectomized (ADX) and sham-operated control rats. AVP-sensitive adenylate cyclase (ADC) activity in PCD did not differ between control and ADX rats. cAMP-phosphodiesterase activity (cAMP-PDIE), measured at 10(-6) M cAMP substrate concentration, was significantly higher (delta + 31.6%) in PCD of ADX rats compared with controls. Incubation of intact PCD from ADX rats with AVP resulted in an accumulation of cAMP (delta - 48.5%) significantly lower than observed in control PCD. Chronic administration of dexamethasone reduced cAMP-PDIE activity in PCD of ADX rats to levels close to or below those observed in control rat PCD, and also resulted in a restoration of AVP-stimulated cAMP accumulation to levels approaching control values. Results indicate that the impaired maximal urinary concentrating ability associated with adrenal insufficiency may be due, at least in part, to a reduced accumulation of cAMP in response to AVP in the PCD. This decreased cAMP accumulation results from increased cAMP-PDIE activity in the PCD of ADX rats and can be corrected by administration of glucocorticoid.
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PMID:Concentrating defect in the adrenalectomized rat. Abnormal vasopressin-sensitive cyclic adenosine monophosphate metabolism in the papillary collecting duct. 630 13

Participation of vasopressin and the renin-angiotensin system in the maintenance of systemic arterial pressure was evaluated in unanesthetized adrenalectomized rats. Adrenalectomized and sham-operated rats with implanted arterial and venous catheters were given 1% sodium chloride and 2.5% glucose as drinking fluid for 72 hours following adrenalectomy. Serum and urine samples were obtained for measurement of electrolyte and solute concentration. The pattern of serum electrolytes, serum osmolality, and renal excretion of electrolytes, solute, and water observed in the adrenalectomized rats was entirely consistent with previous observations in this model. Mean arterial pressure of unanesthetized unrestrained adrenalectomized rats was significantly lower than controls. In adrenalectomized rats, dPMeTyrAVP reduced mean arterial pressure 9 +/- 1 mm Hg, p less than 0.001; captopril then caused an additional reduction of 17 +/- 2 mm Hg, p less than 0.01. Neither antagonist altered arterial pressure in the control group. Our results indicate that vasopressin and the renin-angiotensin system play a compensatory pressor role in adrenal insufficiency, preventing a larger decrease of arterial pressure in this model of chronic hypotension.
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PMID:Maintenance of arterial pressure by vasopressin and angiotensin II after adrenalectomy. 665 64

The effect of adrenal insufficiency on the plasma concentrations of two vasoactive hormones, vasopressin and angiotensin II, was studied in conscious dogs. In addition the role of vasopressin in the maintenance of blood pressure during adrenal insufficiency was studied using [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin, a specific antagonist of the vasoconstrictor action of vasopressin. Dogs were bilaterally adrenalectomized and maintained on daily cortisol and deoxycorticosterone acetate injections. Withdrawal of steroids for 4 days resulted in a 4-fold increase in plasma vasopressin concentration (P less than 0.05) and a 3-fold increase in plasma angiotensin II concentration (P less than 0.001); mean arterial pressure did not change significantly. Administration of the vasopressin antagonist in adrenalectomized dogs maintained on steroids had no effect on blood pressure. In marked contrast, vasopressin blockade in dogs with adrenal insufficiency decreased mean arterial pressure by 22 +/- 5 mm Hg (P less than 0.001). These results demonstrate the plasma angiotensin II and vasopressin concentrations increase during adrenal insufficiency in conscious dogs, and that vasopressin plays an important role in blood pressure regulation in this hypovolemic state.
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PMID:Role of vasopressin in blood pressure regulation during adrenal insufficiency. 684 19


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