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)

Plasma ACTH (normal value: 0.16 plus or minus mU/100 ml) was measured in 116 patients with Cushing's syndrome, using a bioassay including dynamic tests and sequential determinations. In 10 patients with adrenal tumors ACTH levels were nondetectable (ND) or low, and usually nonstimulatable. In 10 patients with ectopic ACTH secretion high levels (0.42 plus or minus 0.07 mU/100 ml) were measured. The extracts of 6 tumors yielded an ACTH-like substance. Forty-three patients with Cushing's disease (without pituitary tumor) had, before treatment, a mean ACTH level of 0.18 plus or minus 0.01 mU/100 ml, accompanied by high levels of plasma cortisol (32.1 plus or minus 1.9 mug/100 ml). Irregular nycthemeral variations occurred. ACTH rose to 0.30 mU/100 ml after incomplete adrenalectomy (20 patients) and to 1.14 mU/100 ml after total adrenalectomy (21 patients). Dexamethasone (8 mg per day) suppressed ACTH levels. Metyrapone induced a normal ACTH rise, but at abnormal times. Lysine-vasopressin (LVP) induced an ACTH mean relative increase of 120% before, and of 140% after adrenalectomy (i.e., within the normal range). Six nonadrenalectomized patients with pituitary tumors showed similar abnormalities of ACTH regulation. However, the ACTH rise after LVP was above 500%. When pituitary tumors occurred after adrenalectomy (12 patients) the mean basal ACTH level was 18 mU/100 ml. Dexamethasone induced a 90% decrease, and LVP a 416% increase in ACTH levels. In 6 patients with nodular adrenal hyperplasia, ACTH was undetectable before treatment. After adrenalectomy, ACTH rose to 0.4 mU/100 ml (11 patients) and the increase after LVP was 90%. Five additional patients developed pituitary tumors. These data confirm the abnormalities of ACTH feedback regulation in Cushing's disease. However, even when pituitary tumors occur, ACTH levels can be altered by metyrapone, dexamethasone and LVP. This last test is of particular interest for the detection of pituitary tumors. The follow-up pattern of treated nodular adrenal hyperplasia appears to be very similar to that of Cushing's disease.
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PMID:Studies of ACTH secretion control in 116 cases of Cushing's syndrome. 16 70

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

A 53-yr-old man with Cushing's disease was found to have a pituitary carcinoma with metastases to the liver and lung which produced both CRH and ACTH simultaneously. Despite removal of the pituitary tumor, his Cushing's disease worsened. Endocrinological examination then demonstrated elevated plasma CRH and markedly elevated plasma ACTH, beta-lipotropin, and cortisol concentrations, increased urinary 17-hydroxycorticosteroid and 17-ketosteroid excretion, and no suppression of serum cortisol after low or high dose dexamethasone administration. Urinary 17-hydroxycorticosteroid excretion increased in response to metyrapone, and lysine vasopressin elicited a striking increase in plasma ACTH. A computed tomographic scan of abdomen revealed multiple hypodense areas in the liver and bilateral adrenal hyperplasia. Postmortem histological examination revealed a necrotic hemorrhagic pituitary carcinoma with metastases to the liver, lung, and olfactory bulb. Immunohistochemical staining, gel filtration, and Northern blot analysis of liver and lung metastases revealed evidence of the production of both CRH and ACTH in these metastases. We concluded that the patient's pituitary carcinoma produced both CRH and ACTH.
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PMID:Corticotropin-releasing hormone- and adrenocorticotropin-producing pituitary carcinoma with metastases to the liver and lung in a patient with Cushing's disease. 169 98

The long-term results of surgical and specific drug therapy were compared in a group of 57 patients with primary aldosteronism (PA) (46 with aldosterone-producing adenoma (APA), 11 with idiopathic hyperaldosteronism (IHA) and bilateral adrenal hyperplasia). Unilateral adrenalectomy completely normalized blood pressure (BP) in 77.1% of surgically treated APA, evidently improving hypertension in remaining 22.9%. No recurrence of the adenoma in the remaining adrenal was seen in any of the surgical APA cases. In 19 of the non-surgical patients (11 with APA, 8 with IHA) monotherapy with spironolactone reduced blood pressure in 73%, though total BP normalization was an exception. The treatment normalized hypokalemia, low total exchangeable potassium, tendency to hypernatremia, and high total exchangeable sodium. Surgical as well as conservative therapy increased to normal or above-normal levels plasma renin activity suppressed prior to treatment. Pre-operatively high urine and plasma aldosterone levels normalized in all adrenalectomized patients, but remained above the normal range during spironolactone therapy in spite of a small decline in its absolute values. The disturbances of maximum renal concentrating capacity due to impaired nephron responsiveness to sufficiently high endogenous vasopressin concentrations were completely eliminated after kaliopenic nephropathy had been repaired. The other renal functions remained within normal values. Echocardiographically diagnosed left ventricular hypertrophy was seen less often than in the other types of arterial hypertension, tending to regress after APA management. Our longitudinal study (2-16 years) showed primary aldosteronism as a well curable, albeit rare, cause of hypertension. As regards BP and laboratory tests normalization, better results were achieved in surgical APA cases than in patients treated with spironolactone. Older age, longer history of hypertension and more frequent incidence of obesity, nephrosclerosis and pyelonephritis may be responsible for hypertension persisting after surgical treatment.
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PMID:Long-term results of surgical and conservative treatment of patients with primary aldosteronism. 345 May 33

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

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

Prolonged use of glucocorticoids (GCs) can cause prolonged suppression of the hypothalamus-pituitary-adrenal (HPA) axis. This study examined the possibility that corticotropin or its secretagogues such as vasopressin, corticotropin-releasing hormone (CRH), or insulin accelerate recovery of the HPA axis after prolonged treatment with dexamethasone (DEX). Suppression of the HPA axis was induced in rats by DEX at a dosage of 250 micrograms/100 g body weight (BW)/d for 14 days, after which rats were administered saline, corticotropin (Cortrosyn 0.1 mg), ovine CRH (oCRH 6 micrograms), vasopressin (2 U), or insulin (2 U) each morning. Adrenal weight (AW), BW, plasma corticosterone, and corticotropin, as well as pituitary corticotropin content, decreased significantly after DEX treatment. The plasma corticotropin level was significantly elevated 7 days after discontinuation of DEX treatment (day 8) and remained so until day 11, whereas the pituitary corticotropin content had returned to normal on day 8. Plasma corticosterone was suppressed until day 8, but was not significantly different from normal on day 11. The AW was also decreased until day 4, but was not different from normal on day 8 or day 11. The BW of experimental rats remained subnormal during the study period. Treatment of DEX-suppressed rats with exogenous corticotropin induced adrenal hyperplasia, but suppressed the plasma corticotropin level and delayed the normalization of plasma corticosterone until day 11. The insulin-treated group differed in no respect from the saline-treated group. Treatment with oCRH or vasopressin for 8 days normalized plasma and pituitary corticotropin, as well as plasma corticosterone. Hypothalamic immunoreactive CRH (iCRH) did not differ among any treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Corticotropin secretagogues facilitate recovery of the hypothalamus-pituitary-adrenal axis suppressed by prolonged treatment with dexamethasone. 817 41

In the last decade, two types of genes participating in the etiology of hypertension have been identified. The primary genes or blood pressure regulators are those that codify enzymes (renin, kallikrein, kininase, aminopeptidase), hormones (angiotensins, vasopressin, aldosterone, prostaglandins, and atrial natriuretic peptide) and substrates (angiotensinogen and kininogen). They cause arteriolar vasodilation or vasoconstriction or sodium retention in the extravascular space. Allelic polymorphisms associated to essential hypertension have been described. The secondary genes are those that produce hereditary diseases of low prevalence, associated to hypertension in 20 to 80% of patients (polycystic kidney disease, pheochromocytoma, adrenal hyperplasia, hereditary nephritis). Forty genes located in all chromosomes, that are dominantly, recessively or X-linked transmitted, have thus far been identified. Chromosomal maps with all genic loci are presented.
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PMID:[The genes of human hypertension]. 946 Feb 75

The aetiology of ACTH-independent macronodular adrenal hyperplasia (AIMAH) is uncertain. We examined a 55 year old man with Cushing's syndrome due to AIMAH, whose cortisol levels increased after stimulation with lysine-8-vasopressin (LVP) in vitro as well as in vivo. Abdominal MRI revealed nodular enlargement of both adrenal glands. No adenoma was evident on pituitary MRI. 131I-adosterol scintigraphy exhibited marked uptake into both adrenal glands. Although baseline plasma cortisol levels were within normal limits, urinary free cortisol excretion was 3-fold higher than the upper limit of the normal range. Plasma ACTH levels were undetectable. Oral dexamethasone failed to suppress plasma cortisol levels irrespective of dose, and administration of corticotrophin releasing hormone failed to increase plasma ACTH and cortisol levels. LVP injection failed to increase plasma ACTH levels, but elicited an increase in plasma cortisol levels. The direct stimulatory effect of LVP on cortisol secretion was confirmed in vitro in cultured adrenocortical cells from macronodules obtained at surgery. Food intake, gastric inhibitory polypeptide (GIP), or octreotide administration, which were reported to regulate cortisol release in patients with AIMAH, failed to affect plasma cortisol levels. In conclusion, plasma cortisol responsiveness to LVP, GIP, and octreotide is heterogeneous in patients with AIMAH.
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PMID:Adrenocorticotrophin-independent macronodular adrenal hyperplasia in a patient with lysine vasopressin responsiveness but insensitivity to gastric inhibitory polypeptide. 949 82

The initial description of GIP-dependent Cushing's syndrome suggested that abnormal or ectopic expression of adrenal receptors for various ligands may underlie other cases of ACTH-independent hypercortisolism. GIP-dependent Cushing's syndrome has been described in patients with unilateral adenomas or bilateral ACTH-independent macronodular adrenal hyperplasia (AIMAH) and results from the adrenal overexpression of non-mutated GIP receptor. In AIMAH, other patients were identified in whom regulation of cortisol production resulted from an abnormal adrenocortical response either to vasopressin, beta-adrenergic receptor agonists, hCG/LH, or serotonin 5-HT-4 receptor agonists. 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 receptor.
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PMID:Abnormal expression and function of hormone receptors in adrenal Cushing's syndrome. 988 84


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