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)

In order to know the pituitary reserves of ACTH, GH, LH, FSH, TSH and prolactin in patients with Cushing's syndrome, the responses of these hormones to hydrocortisone, lysine-8 vasopressin (LVP), insulin-induced hypoglycemia, luteinizing hormon-releasing hormone (LH-RH) and thyrotropin releasing hormone (TRH) were examined before and after treatment. Fourteen patients with Cushing's disease (adrenal hyperplasia), 3 patientswith adrenal adenoma and one patient with adrenal carcinoma were investigated. Before treatment, sufficient response of plasma ACTH to LVP was observed in patients with Cushing's disease, while no response was observed in 3 patients with adrenal adenoma. There was no significant difference in the responses of other pituitary hormones between the patients with Cushing's disease. and the patients with adrenal adenoma. The response of plasma GH to insulin-induced hypoglycemia was impaired in most these patients. The response of plasma TSH to TRH was impaired in 6 of 8 patients tested. The response of plasma LH and FSH to LH-RH were preserved in 6 and 5 of 8 patients, respectively. The response of plasma prolactin to TRH was normal in most patients tested. After treatment, the improvements of the impaired responses of GH, TSH, LH and FSH wereobserved. Therefore, the impaired reserve observed in these patients before treatment seemed to be due to the hypercortisolemia. If the difference of the suppressibility of these pituitary hormones by cortisol may be judged simply from our observation, the orderof the suppressibility is supposed to be ACTH, GH, TSH, LH and FSH, and then prolactin.
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PMID:The pituitary ACTH, GH, LH, FSH, TSH and prolactin reserves in patients with Cushing's syndrome. 80 44

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

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

Cushing's syndrome occurs rarely; in analyzing 50 cases studied at our institution we discuss the following aspects: syndromatic diagnosis, etiologic differentiation into the 3 categories of the syndrome, and therapeutic strategies for each variety. We postulate that non-endocrinologists should be responsible for the syndromatic diagnosis, easily done by using 2 simple tools: the measurement of basal free urinary cortisol and the performance of an overnight suppression of the adrenal axis with 1 mg of dexamethasone (Nugent's test). In contrast, the etiologic diagnosis and the therapeutic interventions should be strictly restricted to highly specialized institutions having well seasoned endocrinologists, a reliable endocrine laboratory, easy access to computed tomographies of the brain and abdomen as well as to nuclear resonance imaging of the brain. The usefulness of our in-house devised vasopressin challenge following overnight dexamethasone suppression for the etiologic diagnosis is highlighted. Neurosurgical expertise in the transsphenoidal approach to the pituitary gland as well surgeons well experienced in adrenal surgery are a must to offer a reasonable chance of success to patients with the syndrome. Forty one (82%) of the series were female patients, 78% were pituitary-dependent and 22% pituitary-independent Cushings. Six out of 8 (75%) of the adrenal tumors were carcinomas. Only 3 patients (6%) qualified as ectopic ACTH syndromes. The easiest variety to diagnose and treat was the adrenal adenoma (2 cases); adrenal carcinomas were always incurable. The ectopic ACTH syndrome was amenable to successful medical treatment with ketoconazole or surgical resolution with complete resection of the offending tumor (1 of 3 cases) or bilateral adrenalectomy (2 of 3 cases) Pituitary-dependent Cushings are quite tricky to diagnose and difficult to treat. Transsphenoidal resection of the offending microadenoma was successful in only 43.5% (10/23) of cases and we experienced 3 recurrences of the syndrome even after 8 years of successful removal of the pituitary adenoma. The remainder had to be cured by bilateral adrenalectomy. Seven out of 39 patients with Cushing's disease (18%) ultimately died for a variety of reasons; six out of 6 patients (100%) with adrenal carcinoma died of dissemination; two out of 2 adrenal adenomas cured and 1 out of the 3 ectopic ACTH syndromes died of dissemination of a malignant thymic carcinoma. We conclude that Cushing's syndrome is a serious, underdiagnosed disorder, which should be suspected and diagnosed by the non specialized physician and then referred to a specialized center for expert etiologic diagnosis and surgical therapy.
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PMID:[Cushing's syndrome: review of a national caseload]. 852 77

Recent studies from several groups have indicated that abnormal or ectopic expression and function of adrenal receptors for various hormones may regulate cortisol production in ACTH-independent hypercortisolism. Gastric inhibitory polypeptide (GIP)-dependent Cushing's syndrome has been described in patients with either unilateral adenoma or bilateral macronodular adrenal hyperplasia; this syndrome results from the large adrenal overexpression of the GIP receptor without any activating mutation. We have conducted a systematic in vivo evaluation of patients with adrenal Cushing's syndrome in order to identify the presence of abnormal hormone receptors. In macronodular adrenal hyperplasia, we have identified, in addition to GIP-dependent Cushing's syndrome, other patients in whom cortisol production was regulated abnormally by vasopressin, ss-adrenergic receptor agonists, hCG/LH, or serotonin 5HT-4 receptor agonists. In patients with unilateral adrenal adenoma, the abnormal expression or function of GIP or vasopressin receptor has been found, but the presence of ectopic or abnormal hormone receptors appears to be less prevalent than in macronodular adrenal hyperplasia. The identification of the presence of an abnormal adrenal receptor offers the possibility of a new pharmacological approach to control hypercortisolism by suppressing the endogenous ligands or by using specific antagonists for the abnormal receptors.
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PMID:The diversity of abnormal hormone receptors in adrenal Cushing's syndrome allows novel pharmacological therapies. 1100 21

Recent studies from several groups have indicated that abnormal or ectopic expression and function of adrenal receptors for various hormones may regulate cortisol production in ACTH-independent hypercortisolism. GIP-dependent Cushing's syndrome has been described in patients with either unilateral adenomas or bilateral macronodular adrenal hyperplasia; this syndrome results from the adrenal overexpression of the GIP receptor, which was found to be without an activating mutation. An increased stimulation of cortisol secretion following administration of vasopressin was also reported by several investigators in patients with adrenal Cushing's syndrome; this was linked to an increased expression or abnormal response of the V1-vasopressin receptor. We have conducted a prospective in vivo evaluation of 20 patients with adrenal Cushing's syndrome in order to identify the presence of abnormal hormone receptors. In 6 cases of macronodular adrenal hyperplasia, we have identified, in addition to 2 cases of GIP-dependent Cushing's syndrome, 4 other patients in whom cortisol production was regulated abnormally either by vasopressin, B-adrenergic receptor agonists, hCG/LH, or serotonin 5-HT-4 receptor agonists. In 13 patients with unilateral adrenal adenoma, an abnormal response to a mixed meal or to vasopressin was found in 3 cases, suggesting that the presence of ectopic or abnormal hormone receptors is less prevalent than in macronodular adrenal hyperplasia. The identification of the presence of an abnormal adrenal receptor offers the possibility of a new pharmacological approach to control hypercortisolism by suppressing the endogenous ligands or by using specific antagonists of the abnormal receptors.
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PMID:[Illicit hormone receptors in adrenal Cushing's syndrome]. 1135 92

Arginine vasopressin (AVP) stimulates cortisol secretion through its vascular type V(1a) receptor in the adrenal glands, in addition to stimulating ACTH secretion through pituitary V(3) receptor. Because hyper-response of plasma cortisol to vasopressin is documented in some patients with Cushing's syndrome due to adrenal adenoma (CS) or ACTH-independent macronodular adrenocortical hyperplasia (AIMAH), we analyzed the expression of V(1a), V(2), V(3) receptor and AVP mRNA in human adrenal tissues by quantitative competitive RT-PCR or real-time PCRs. V(1a) receptor mRNA levels (ratio against glyceraldehyde 3-phosphate dehydrogenase) were 0.378 +/- 0.143 (mean +/- SE) in preclinical CS (n = 5) and 0.630 +/- 0.072 in AIMAH (n = 4), which were significantly higher than those (0.046 +/- 0.012; n = 9) in control adrenals, whereas those in overt CS (0.143 +/- 0.048; n = 10) or aldosterone-producing adenomas (0.069 +/- 0.018; n = 12) were similar to control adrenals. Although ectopic expression of V(2) or V(3) receptor was detected in half of AIMAH cases, the absolute levels were low. Furthermore, V(1a) receptor mRNA levels in the adjacent adrenal glands (0.190 +/- 0.039, n = 9) of aldosterone-producing adenomas were higher than those in control adrenals and in the corresponding tumor portions (0.079 +/- 0.024). In contrast, there were no significant differences in AVP mRNA levels among these groups. These results suggest that eutopic V(1a) receptor overexpression is involved in the etiology of AIMAH and a subset of adrenal adenomas causing overt or preclinical Cushing's syndrome. Our results imply a possible association of V(1a) receptor expression with adrenal hyperplasia.
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PMID:Eutopic overexpression of vasopressin v1a receptor in adrenocorticotropin-independent macronodular adrenal hyperplasia. 1246 75

Regulation of cortisol secretion by aberrant hormone receptors may play a role in the pathogenesis of ACTH-independent Cushing's syndrome. In this study, the topic was evaluated by combining in vivo and in vitro approaches. Cortisol responses to various stimuli (standard meal, GnRH + TRH, cisapride, vasopressin, glucagon) were assessed in 6 patients with clinical or subclinical adrenal Cushing's syndrome, and non-functioning adrenal adenoma in two cases. Abnormal responses were observed in three patients with Cushing's syndrome; one patient showed a gastric inhibitory polypeptide (GIP)-dependent cortisol rise after meal, together with responses after GnRH and cisapride; the second patient showed an LH-dependent cortisol response to GnRH, and in the third cortisol rose after cisapride. The pattern of receptor expression performed by RT-PCR showed that while GIP-R was only expressed in tumor from the responsive patient, 5-hydroxytryptamine type 4 receptor and LH-R were also present in normal adrenal tissues and tissues from non-responsive patients. Interestingly, an activating mutation of Gsalpha gene was identified in one of these tumors. Therefore, cortisol responses to agents operating via Gs protein coupled receptors (in one case associated with Gsalpha mutation) were found in Cushing's patients, while these responses were absent in the others. The finding of receptor expression in normal and non-responsive tumors suggests that different mechanisms are probably involved in inducing in vivo cortisol responses.
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PMID:Assessing the presence of abnormal regulation of cortisol secretion by membrane hormone receptors: in vivo and in vitro studies in patients with functioning and non-functioning adrenal adenoma. 1613 68

Endogenous Cushing's syndrome is a clinical state resulting from prolonged, inappropriate exposure to excessive endogenous secretion of cortisol and hence excess circulating free cortisol, characterized by loss of normal feedback mechanisms of the hypothalamo-pituitary-adrenal axis and normal circadian rhythm of cortisol secretion. The etiology of Cushing's syndrome may be excessive ACTH secretion from the pituitary gland, ectopic ACTH/CRH secretion by non-pituitary tumor, or excessive autonomous secretion of cortisol from hyperfunctioning adrenal adenoma or carcinoma, PPNAD and MAH. Other than these broad ACTH-dependent and ACTH-independent categories, there are some unclassified variants as cyclical Cushing's syndrome, pituitary hyperplasia and subclinical Cushing's syndrome. In addition, variants of hypercorticism secondary to ectopic or aberrant expression of several G-protein-coupled receptors have been identified. Diagnosis of Cushing's syndrome must be made before any attempt at differential diagnosis, and key biochemical characteristics are: excess endogenous cortisol secretion; loss of normal feedback of hypothalamic-pituitary-adrenal axis; and disturbance of normal circadian rhythm of cortisol secretion. Biochemical diagnosis of Cushing's syndrome includes: urinary free cortisol determination, low-dose dexamethasone testing, circadian rhythm assessment, insulin tolerance test, and LDDST/CRH test. Differential diagnosis of Cushing's syndrome involves: plasma ACTH level determination, high dose dexamethasone testing, metyrapone testing, testing with CRH, testing with vasopressin or combination, and finally, bilateral simultaneous petrosal sinus sampling with CRH stimulation.
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PMID:[Diagnosis and differential diagnosis of Cushing's syndrome]. 1730 74

Aldosterone-producing adrenal adenoma can induce various clinical manifestations as a result of chronic exposure to aldosterone. We report a rare case of a 37-year-old man who complained of general weakness and polyuria. He was diagnosed with aldosterone-producing adrenal adenoma and nephrogenic diabetes insipidus. Aldosterone enhances the secretion of potassium in the collecting duct, which can lead to hypokalemia. By contrast, nephrogenic diabetes insipidus, which manifests as polyuria and polydipsia, can occur in several clinical conditions such as acquired tubular disease and those attributed to toxins and congenital causes. Among them, hypokalemia can also damage tubular structures in response to vasopressin. The patient's urine output was >3 L/d and was diluted. Owing to the ineffectiveness of vasopressin, we eventually made a diagnosis of nephrogenic diabetes insipidus. Laparoscopic adrenalectomy and intraoperative kidney biopsy were subsequently performed. The pathologic finding of kidney biopsy revealed a decrease in aquaporin-2 on immunohistochemical stain.
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PMID:A case of primary aldosteronism combined with acquired nephrogenic diabetes insipidus. 2688 83


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