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

ACTH and lipotropins (beta- and gamma-LPH) are synthesized from a common precursor by the pituitary corticotropic cell. We have measured LPH plasma levels under physiological and pathological conditions and we have compared them with ACTH plasma levels in the same circumstances. Spontaneous variations (nycthemeral rhythm) in LPH, ACTH and cortisol plasma levels were parallel, while responses to Dexamethasone freination test and stress (Insulin induced hypoglycemia) or more specific stimulation (Metopirone, lysine-vasopressin) were parallel and superimposable. LPH levels were always higher than ACTH levels in two pathological circumstances: chronic renal failure and Cushing's syndromes with ectopic ACTH producing tumors. The determination of both ACTH and LPH levels assists the diagnosis of corticotropic insufficiency and etiologic investigation of Cushing's syndrome, after hypercorticolism had been established. Although unable to confirm the presence of corticotropic adenoma in patients with Cushing's disease, or the predict effectiveness of pituitary surgery, these determination bring good arguments for treated Cushing's diseases follow up.
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PMID:[ACTH, beta-endorphin and lipotropins: physiopathological studies in man (author's transl)]. 628 91

Direct effects of cyproheptadine, reserpine, synthetic ovine corticotropin-releasing factor (CRF), dexamethasone, and lysine-8-vasopressin (LVP) on the secretion of immunoreactive ACTH and beta-endorphin from the adenoma and the nonadenomatous tissue of patients with Cushing's disease were examined using a superfusion system. Cyproheptadine and reserpine (10(-9)-10(-7) M of each) suppressed immunoreactive ACTH and beta-endorphin secretion from both tissues. CRF (10(10)-10(7) M) stimulated the secretion of both peptides from the nonadenomatous tissue, but only a high dose of CRF could stimulate the secretion of these peptides from some adenomas. Such CRF-induced secretion was partially suppressed by dexamethasone. LVP (10(-9)-10(-7) M) stimulated peptide secretion from both types of tissue. These results suggest direct inhibitory effects of cyproheptadine and reserpine on the secretion of these peptides from the pituitary of patients with Cushing's disease, a different stimulatory mechanism of LVP from that of CRF in these tissues, and low sensitivity of the adenoma to CRF.
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PMID:Effects of cyproheptadine, reserpine, and synthetic corticotropin-releasing factor on pituitary glands from patients with Cushing's disease. 630 23

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 three female patients with Cushing's disease, 100 micrograms of synthetic ovine corticotropin releasing factor (CRF) were administered before surgery and 1 week after transsphenoidal microadenomectomy. In these patients a test with lysine-vasopressin (LVP), 10 U intramuscularly, was also performed before and after pituitary surgery. Before surgery, both stimuli induced a clear increase in plasma ACTH and cortisol in all patients; the response of ACTH to CRF was of greater magnitude. Postoperatively, the responses were virtually absent in two patients, but were still present in the third one in whom the removal of adenoma had been partially unsuccessful. The CRF test was also performed in a female patient with Cushing's syndrome due to adrenal adenoma; in this patient no responses of plasma ACTH and cortisol to CRF were recorded. This paper demonstrates that pituitary microadenomas causing Cushing's disease may retain the ability to respond to CRF; this stimulus may be useful in the differential diagnosis between ACTH-dependent and independent Cushing's syndrome; the lack of response after microadenomectomy indicates successful removal of the tumor. CRF is more potent than LVP in releasing ACTH at the doses employed.
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PMID:Plasma ACTH-response to the corticotropin releasing factor in patients with Cushing's disease. Comparison with the lysine-vasopressin test. 632 50

Dispersed corticotrophic cells of 3 patients with Nelson's syndrome were studied in tissue culture for up to 25 days. During this culture period a parallel decrease with time was seen in ACTH and beta-endorphin-like immunoreactivity ( LIR ) release. A concomitant decline was observed for intracellular hormones. The time course of hormone release showed a parallel secretion of ACTH and beta-endorphin- LIR up to 8 h. Both the release of ACTH and beta-endorphin LIR were stimulated by 0.1 microM lysine vasopressin (LVP) in all three adenoma cell cultures. Dexamethasone (0.1 and 1 microM) suppressed basal hormone secretion for 4 h. Synthetic ovine corticotrophin-releasing factor (CRF) at 10 and 100 nM stimulated the secretion of ACTH and beta-endorphin LIR maximally. This stimulation was higher than observed with maximal stimulative concentration of LVP (0.3 microM). The CRF-mediated hormone secretion was calcium-dependent. Dexamethasone (0.1 microM) blocked the stimulating effect of 10 nM CRF completely. Gel-filtration chromatography demonstrated the cells to secrete both beta-lipotrophin (beta-LPH) and beta-endorphin. The ratio of beta-LPH to beta-endorphin released remained constant upon stimulation by LVP and CRF. HPLC studies demonstrate the possibility that several beta-endorphin fragments, including alpha-endorphin and gamma-endorphin, were secreted by cells from a Nelson tumour. CRF caused a simultaneous parallel stimulation of the release of these peptides.
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PMID:ACTH and beta-endorphin secretion by three corticotrophic adenomas in culture. Effects of culture time, dexamethasone, vasopressin and synthetic corticotrophin releasing factor. 632 19

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

We present two patients with Cushing's syndrome due to ACTH-independent macronodular adrenal hyperplasia who showed marked plasma cortisol response to lysine-8-vasopressin (LVP) injection (from 930 and 731 pmol/L to 2177 and 1920 pmol/L, respectively), while plasma ACTH levels remained undetectable. The ACTH independence of cortisol secretion in the two patients was determined from the following endocrinological findings. Plasma cortisol levels were not increased by corticotropin-releasing hormone injections and were not suppressed by high dose (16 mg) dexamethasone administrations. The plasma ACTH levels, measured by two independent sensitive immunoassays, were persistently undetectable even after corticotropin-releasing hormone injection, metyrapone administration, and bilateral adrenalectomy. The particular pathological finding of the two cases, atrophic lesions in nonnodular parts of the adrenal cortexes, also indicated ACTH independence of the macronodular hyperplasia. In vitro examination revealed a direct effect of LVP on cortisol secretion from the adrenal cells of the macronodules. We also examined seven patients with Cushing's syndrome caused by adrenal adenoma and found a statistically significant plasma cortisol response to LVP injection. The direct effect of LVP was also demonstrated in cultured adenoma cells. In conclusion, we discovered a direct adrenal effect of LVP on cortisol secretion in patients with ACTH-independent macronodular hyperplasia and, to a lesser extent, in patients with cortisol-producing adrenal adenoma. The cortisol response to LVP may serve to facilitate their diagnosis and choice of therapy.
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PMID:Lysine vasopressin stimulation of cortisol secretion in patients with adrenocorticotropin-independent macronodular adrenal hyperplasia. 762 26

We report a case of a Cushing's syndrome caused by an autonomously secreting unilateral adrenocortical tumor, characterized by a clinically and biologically mild hypercortisolemic state and an unusual response pattern to vasopressin. Laboratory tests showed normal early morning plasma cortisol and 24-h urinary cortisol excretion, but lack of nycthemeral variations and suppressed plasma ACTH. Urinary cortisol excretion was not suppressed by either the low dose or the high dose dexamethasone test. Injection of lysine vasopressin, (10 IU, im) induced a marked increase in plasma cortisol, without an elevation of plasma ACTH. Computed tomography scan revealed an adrenocortical mass of the left gland with a contralateral atrophic gland. Removal of the tumor led to complete remission of Cushing's symptoms. In vitro studies were then performed to investigate the effect of arginine vasopressin (AVP) on calcium mobilization in cultured tumor cells using a microfluorimetric technique. Application of AVP in the vicinity of the cells induced a rapid and marked increase in the intracellular calcium concentration. Preincubation of the cells with the V1 vasopressin receptor antagonist [d(CH2)5,Tyr(OMe)2]AVP totally suppressed the AVP-induced stimulation of intracellular calcium concentration. Reverse transcription followed by polymerase chain reaction of tumor ribonucleic acid with specific oligonucleotides amplified high levels of V1 receptor signal compared with normal adrenocortical ribonucleic acid. Specific oligonucleotides for the V2 or V3 receptors amplified only a faint signal. This is the first report describing a mild case of Cushing's syndrome caused by an AVP-sensitive cortisol-producing adenoma. The direct effect of AVP on cultured tumor cells was mediated through the V1 type of vasopressin receptor, similar to that previously characterized in normal human fasciculata cells, suggesting that the tumor expressed an eutopic V1 AVP receptor and exhibited overresponsiveness to AVP.
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PMID:Vasopressin-responsive adrenocortical tumor in a mild Cushing's syndrome: in vivo and in vitro studies. 767 9

This study evaluated the assessment of plasma endothelin-1 (ET-1) levels in primary aldosteronism and its correlation with other vasoactive hormones such as renin, aldosterone, catecholamines, arginine-vasopressin, and atrial natriuretic peptide. Plasma ET-1 was measured in 12 patients with primary aldosteronism (five adenomas and seven primary hyperplasia) and in 15 normal subjects. No significant differences were found in plasma ET-1 between controls and hypertensive patients both in adenoma and primary adrenal hyperplasia (8.8 + 1.6 pg/mL v 6.2 + 1.4 pg/mL v 6.5 + 1.0 pg/mL, P = NS, respectively). Further, no significant correlations were found among ET-1 and vasoactive hormones. In conclusion, these findings show that there are no differences in ET-1 levels between primary aldosteronism patients and healthy subjects. Circulating ET-1 is not involved in the hypertension in primary aldosteronism.
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PMID:Plasma immunoreactive endothelin-1 in primary hyperaldosteronism. 791 56


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