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)

An 18-month old infant with Cushing's disease due to an ACTH producing pituitary tumor is presented. The case showed typical clinical and morphological sings of hypercortisolism. The infant died of pulmonary thromboembolism after transsphenoidal partial adenomectomy. The adrenals were diffusely hyperplastic. The pituitary adenoma was classified as an undifferentiated mucoid cell adenoma with sparse granulation by light microscopy. Immunoenzymatic studies demonstrated ACTH not only in granulated adenoma cells. Ultrastructurally the cells were only differentiated as typical ACTH cells or so-called follicular cells in small areas. Most of them were undifferentiated, showing pleomorphism of the relatively sparse organelles. In-vitro experiments using suspensions of adenoma cells showed a distinct enhancement of ACTH secretion after arginine-vasopressin and a further decrease ultrastructurally in the number of secretory granules. No effect of ACTH levels and no alterations of the ultrastructure were observed after cortisol. The case is representative of typical hypothalamic-hypophyseal Cushing's disease with an undifferentiated pituitary adenoma secreting ACTH in part autonomously. This constellation of Cushing's syndrome is extremely rare at the age of one year. Our case is the second one reported in the literature.
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PMID:ACTH secreting pituitary adenoma in an infant of 18 months. Immunohistochemical, electron-microscopic, and in-vitro studies. 627 57

The effect of D-Ala2, MePhe4, Met-(0)enkephalinol (Sandoz FK 33-824; 0.5 mg, im) on pituitary hormone secretion was studied in 11 patients with Addison's disease and 11 patients with ACTH-dependent Cushing's disease. In patients with Addison's disease, a pronounced fall of plasma ACTH levels was observed (P less than 0.005). The ACTH response to FK 33--824 was partially reversed by naloxone (4 mg, iv). In patients with Cushing's disease, no unequivocal decrease in either ACTH or cortisol was seen. Moreover, FK 33--824 failed to influence the vasopressin-induced ACTH increase in 5 patients with Cushing's disease. In patients with cortisol deficiency due to either Addison's disease or bilateral adrenalectomy for Cushing's disease, FK 33--824 led to increases in PRL and GH similar to those described in normal subjects. However, in the presence of longstanding hypercortisolism, the PRL increase was significantly diminished, and the GH response to FK 33--824 was completely abolished. Our results suggest that in Addison's disease ACTH release is influenced by inhibitory opiate receptors. In patients with Cushing's disease, ACTH secretion is insensitive to FK 33-284, presumably because of an autonomous pituitary adenoma or hypothalamic derangement. The impairment of the PRL and GH responses to FK 33--824 in Cushing's syndrome seems to reflect a direct action of the elevated cortisol level, for it is not seen after bilateral adrenalectomy.
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PMID:Effects of a met-enkephalin analog on adrenocorticotropin (ACTH), growth hormone, and prolactin in patients with ACTH hypersecretion. 628 Dec 97

Administration of cyproheptadine for 2 months to five dogs with pituitary-dependent hyperadrenocorticism (PDH) at a dose rate of 0.3 mg/kg per 24 h (group 1) and to four dogs with PDH at a dose rate of 1 mg/kg per 24 h (group 2) did not result in any clinical improvement. The hyperadrenocorticoid state, as indicated by the circulating cortisol levels, the urinary corticosteroid excretion and the response of the hypothalamo-pituitary-adrenal axis to lysine-vasopressin, thyrotrophin releasing hormone and dexamethasone did not change consistently, although there was a tendency to normalization of some parameters in the dogs of group 2. However, these changes were not found to be consistent for each individual dog but were limited to one parameter per dog. It is concluded that cyproheptadine is not suitable for the treatment of PDH in the dog.
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PMID:Results of cyproheptadine treatment in dogs with pituitary-dependent hyperadrenocorticism. 672 7

Water balance studies were performed in 7 experimental dogs before and during a period of cortisol-induced polyuria and in one dog with spontaneous hyperadrenocorticism before and after removal of an adrenocortical carcinoma. Measurements of urine and plasma osmolality and plasma arginine vasopressin concentration were made at regular intervals during the water deprivation studies. The results indicate that cortisol does not block the release of vasopressin but interferes with its action in the kidney.
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PMID:Studies on the mechanism of polyuria induced by cortisol excess in the dog. 744 17

An unusual of bilateral adrenal benign adenoma with Cushing's syndrome is reported. Nine months after bilateral adrenalectomy, no more sign of hyperadrenocorticism was present. An adenoma was found in each gland with adjacent tissue atrophic. Physiopathology is not clear even if suppression test by dexamethasone and stimulation test by lysin-vasopressin are compatible with a central origin.
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PMID:[Cushing's syndrome caused by a bilateral adrenal adenoma (author's transl)]. 746 40

In pituitary-dependent hyperadrenocorticism (Cushing's disease), the disturbed regulation of ACTH secretion is associated with neoplastic transformation of corticotropic cells. As these two phenomena are almost indissolubly connected, it is of prime importance to elucidate the factor(s) that induce corticotropic cell proliferation. Here we report on the effects of hypophysiotrophic hormones and intrapituitary growth factors on the proliferation and hormone secretion of the murine corticotropic tumour cell line AtT20/D16v, as measured by DNA content, and ACTH concentration in culture media. In addition, sensitivity to the inhibitory effect of cortisol was assessed under various conditions. Corticotropin releasing hormone (CRH) and vasopressin (AVP) induced proliferation of AtT20-cells. In contrast to that caused by AVP, the CRH-induced proliferation was associated with increased ACTH secretion, which could be inhibited by cortisol. Insulin-like growth factor-I (IGF-I), epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF) also stimulated the proliferation of AtT20-cells. The proliferation of AtT20-cells was significantly inhibited by cortisol in all tests. The IGF-I-induced proliferation was the least sensitive to inhibition by cortisol. The growth factors did not stimulate ACTH secretion but IGF-I differed in that it prevented the inhibition of basal ACTH secretion by cortisol. Additional experiments (Western ligand blot analysis) concerning the relative insensitivity of IGF-I induced proliferation to inhibition by cortisol revealed that IGF-I increased the concentration of a 29 kDa IGF binding protein (IGFBP) in the culture medium. The concentration of the 29 kDa IGFBP was slightly decreased by cortisol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proliferation of the murine corticotropic tumour cell line AtT20 is affected by hypophysiotrophic hormones, growth factors and glucocorticoids. 754 6

Renal phosphate wasting related to a tumor (oncogenous osteomalacia) is a rare disorder usually associated with benign mesenchymal tumors. In this article, the authors describe a man with renal phosphate wasting and the syndrome of inappropriate antidiuretic hormone associated with small cell carcinoma. Chemotherapy markedly reduced tumor burden and was associated with normalization of renal phosphate handling and serum sodium. With recurrence, renal phosphate wasting and the syndrome of inappropriate antidiuretic hormone developed again, with the additional complication of hypercortisolism secondary to ectopic corticotropin production. The authors report the rare occurrence of renal phosphate wasting with small cell carcinoma (5 previously reported cases) and the unique co-existence of this paraneoplastic syndrome with the syndrome of inappropriate antidiuretic hormone and ectopic corticotropin production.
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PMID:Case report: renal phosphate wasting, syndrome of inappropriate antidiuretic hormone, and ectopic corticotropin production in small cell carcinoma. 760 39

Chronic liver disease may be accompanied by disturbed sodium and water homeostasis. There is usually sodium retention and ascites. However, spontaneous natriuresis has also been reported in humans and experimental animals with liver cirrhosis. Chronic hypercortisolism, which may occur in dogs with advanced liver disease, is known to induce the inhibition of the osmostimulation of vasopressin (AVP) release. We have therefore investigated the osmoregulation of AVP release in 11 dogs with chronic hypercortisolism associated with advanced liver dysfunction and hepatic encepahlopathy and in 10 control dogs. Basal pituitary-adrenocortical activity was investigated by measuring the concentration in multiple plasma samples of adrenocorticotropin (ACTH), alpha-melanocyte-stimulating hormone (MSH), and cortisol and the cortisol:creatinine ratio in 24-hr urine. Urine specific gravity was also measured. The feedback regulation of the system was investigated by measuring these hormones in plasma after an intravenous (iv) injection of 0.01 mg/kg of dexamethasone. The osmoregulation of the release of AVP was investigated by the intravenous infusion of a 20% NaCl solution at a flow rate of 0.03 ml/kg for 2 hr and the measurement of AVP in plasma sampled at 20-min intervals. The AVP release was analyzed in terms of the threshold osmolality at which it commenced and the sensitivity, which reflects the magnitude of the response. All dogs had highly increased urinary cortisol:creatinine ratios, ranging from 21 to 210 x 10(-6) (normally < 10 x 10(-6)). The mean basal plasma concentrations of the three pituitary-adrenocortical hormones were significantly increased. ACTH values were 35 to 146 ng/l (normally, 14 to 68), MSH values were 26 to 118 ng/l (normally, 10 to 36), and cortisol values were 88 to 194 nmol/l (normally, 23 to 112). The feedback inhibition of the secretion of ACTH and cortisol in response to dexamethasone was unaffected. Urine specific gravity was significantly decreased. The regulation of AVP release was found to be abnormal in all dogs with hepatic encephalopathy. The osmotic threshold at which the release of AVP was induced was abnormally high in seven of the dogs with liver disease and in the normal range in one. It could not be determined in three dogs. The sensitivity of AVP release in response to increasing plasma hypertonicity was normal in two dogs and decreased in nine. In three dogs, there was no increase in AVP release. None of the dogs had normal values for both the sensitivity and the threshold.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chronic glucocorticoid excess and impaired osmoregulation of vasopressin release in dogs with hepatic encephalopathy. 762 76

Chronic increases in cortisol inhibit basal plasma arginine vasopressin (AVP). Acute pretreatment with cortisol inhibits the large increase in AVP during hypotension or hypoxia but does not inhibit the modest increase in AVP in response to hypertonic saline (HS). We evaluated the effect of a chronic increase in cortisol (physiological range) on the acute AVP response to HS. Five male dogs received a continuous infusion of either vehicle or cortisol (65 mg/day) for 7 days. The AVP response to HS (0.2 mmol.kg-1.min-1 for 30 min) was tested before infusion, on days 1, 4, and 7 of chronic infusion, and 2 days after the infusion was discontinued. Plasma cortisol increased significantly from 1.0 +/- 0.2 micrograms/dl to an average over the 7 days of infusion of 5.0 +/- 0.2 micrograms/dl, and basal plasma AVP was significantly decreased during cortisol infusion. The increase in plasma Na and osmolality during HS was unaffected by chronic infusion. HS resulted in an increase in AVP from 3.5 +/- 0.2 to 7.1 +/- 0.7 pg/ml before cortisol infusion. After 7 days of cortisol, the AVP response to HS (from 2.6 +/- 0.1 to 3.9 +/- 0.7 pg/ml) was significantly attenuated. Sustained, physiological increases in cortisol significantly inhibited osmotically stimulated AVP release. The decrease in AVP during hypercortisolism and the syndrome of inappropriate antidiuretic hormone in patients with adrenal insufficiency appear to be due to an inhibitory effect of cortisol on the osmotic sensitivity of the AVP control system.
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PMID:Chronic physiological increases in cortisol inhibit the vasopressin response to hypertonicity in conscious dogs. 797 63

Glucocorticoid deficiency leads to elevated plasma vasopressin (AVP), while chronic endogenous hypercortisolism may inhibit osmotically stimulated AVP, suggesting that glucocorticoids may be feedback inhibitors of AVP secretion. We evaluated the effect of physiological increases in cortisol (65 mg/day iv) for 7 days on basal AVP and oxytocin (OT) in five conscious, male dogs. Cortisol increased from 1.3 +/- 0.1 to 5.0 +/- 0.8 micrograms/dl during infusion. Basal plasma AVP significantly decreased from 3.5 +/- 0.2 to 2.6 +/- 0.3 pg/ml during cortisol infusion. Plasma OT, osmolality, and sodium did not change while arterial pressure decreased (from 107 +/- 3 to 102 +/- 2 mmHg) on days 4 and 6. Increases in cortisol led to a physiologically significant, nonosmotic decrease in AVP. The effect was specific to AVP and independent of changes in arterial pressure. Glucocorticoid administration significantly decreased basal AVP within 24 h, which is comparable to the negative feedback control of adrenocorticotropic hormone. The inverse relationship between cortisol and AVP may account for the nonosmotic change in AVP in patients with disorders of glucocorticoid secretion.
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PMID:Physiological increases in cortisol inhibit basal vasopressin release in conscious dogs. 802 23


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