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)

The hypothalamic pituitary adrenocortical function has been studied in 16 patients operated from pituitary tumors (13 adenomas; 3 craniopharyngiomas). Comparisons have been made between corticotropin and cortisol response to lysine vasopressin, insulin induced-hypoglycemia and metyrapone IV and per os. Among these different stimulating tests, insulin induced hypoglycemia and metyrapone per os seem to give the more accurate informations metyrapone per os being more convenient because harmless. Three different groups of patients have been distinguished : one without adrenocortical deficiency; one with a complete deficiency and a third group with a partial deficiency. Correlations have been studied between the degree of the adrenocortical deficiency, the volume of the tumor and the presence of the absence of other anterior pituitary dysfunctions.
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PMID:[Study of the hypothalamo-pituitary adrenal function in 16 patients after surgery for pituitary tumor (author's transl)]. 21 1

A 52-year-old woman experienced hypoadrenalism (mean 8 AM plasma cortisol level, 3.7 microgram/dL) after hypothalamic surgery and radiotherapy for craniopharyngioma. Despite low plasma adrenocorticotropic hormone levels (less than 25 pg/mL), absent diurnal variation of the plasma cortisol level, and subnormal urinary 17-hydroxycorticosteroid response to metyrapone, she had normal plasma cortisol responses to insulin-induced hypoglycemia and to administration of vasopressin or synthetic adrenocorticotropic hormone. Stress-induced cortical release may be preserved despite notable abnormalities in regulation of cortisol secretion by diurnal and feedback-mediated mechanisms.
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PMID:Stress-induced cortisol release in hypothalamic hypoadrenalism. 21 66

A patient with hypoadrenocorticism was found to have low basal plasma concentrations of ACTH and lipotropins and deficient responses of these hormones to insulin-induced hypoglycemia and lysine vasopressin. The adequacy of secretion of other anterior pituitary hormones was assessed either directly, by measuring their concentration in plasma, or indirectly, by assessing end organ function, under basal and stimulated conditions. The responses of gonadotropins to LRH and of PRL and TSH to TRH were normal. The etiology of this rare condition of isolated deficiency of ACTH and lipotropins remains to be elucidated.
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PMID:Isolated deficiency of adrenocorticotropin (ACTH) and lipotropins (LPHs). 23 63

Somatotropic, thyrotropic, gonadotropic and corticotropic functions in 10 patients with idiopathic hypopituitary dwarfism (IH) were investigated. The patients were divided into two groups: Group I (5 patients) had normal plasma T4 levels, and Group II (5 patients) had T4 levels of less than 4.6 microgram/dl. In Group I three cases had isolated growth hormone (GH) deficiency and two cases had GH and gonadotropin (Gn) deficiencies; in Group II the 5 cases showed multiple anterior pituitary hormone deficiencies. In Group II, the plasma thyroid stimulating hormone (TSH) was 4.1-9.4 muU/ml and the response to thyrotropin releasing hormone (TRH) was greatly delayed and prolonged, with a maximum after 120 min instead of 15 min. The basal prolactin (PRL) level in Group II was 12-31 ng/ml, which was significantly higher than normal (P less than 0.001). In 4 cases in Group II, the plasma cortisol level increased 120 min after the infusion of lysine-vasopressin, whereas oral administration of metyrapone and hypoglycemia induced by insulin did not increase the plasma cortisol levels. From these findings it is concluded that hypothalamic lesions caused the pituitary hormone deficiencies in 4 Group II cases, and Group I may tentatively be differentiated from Group II by T4 determinations.
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PMID:Hypothalamic-pituitary functions in patients with idiopathic pituitary dwarfism. Further evidence for hypophysiotropic human deficiencies. 67 52

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

The physiological regulation of the plasma corticosteroid concentration, measured by competitive protein-binding, was studied in female rhesus monkeys (M. mulatta) sedated with phencyclidine hydrochloride. Morning basal levels of plasma corticosteroids were found to be in the range 8-0-25-2 mug/100 ml, which is lower than that previously reported in this species. A circadian rhythm in plasma cortisol concentration was demonstrated. Prolonged sedation with phencyclidine was associated with a gradual increase in the plasma cortisol concentration. Synthetic alpha1-24 adrenocorticotrophic hormone given intravenously caused a rapid rise in plasma cortisol, the minimum effective dose was between 1 and 10 ng/kg body weight and the response was maximal after 1000 ng/kg. The administration of lysine-vasopressin and the induction of hypoglycaemia by insulin were both followed by an increase in the plasma corticosteroid concentration. Metyrapone caused a decline in plasma 11-hydroxycorticosteroids and a concomitant increase in total corticosteroids measured by competitive protein-binding. It is concluded that the hypothalamic-pituitary-adrenal system in the rhesus monkey functions in a manner which is qualitatively and quantitatively similar to that of man.
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PMID:Studies on plasma corticosteroids in the rhesus monkey (Macaca mulatta). 81 35

Six patients with vasopressin-responsive diabetes insipidus (DI) received clofibrate and chlorpropamide, singly and in combination. Decrease in urinary output averaged (mean +/- SEM): (1) clofibrate 2 g/day, 47% +/- 6%; (2) chlorpropamide 250 mg/day 59% +/- 5%; (3) clofibrate 2 g/day plus chlorpropamide 125 mg/day, 54% +/- 7%; (4) clofibrate 2 g/day plus chlorpropamide 250 mg/day 61% +/- 4%. Water deprivation tests before and during treatment showed significantly higher basal, final, and peak urinary osmolalities (Uosm) and lower free water clearance (CH20) on chlorpropamide, singly and in combination: clofibrate raised Uosm less but significantly decreased CH2O. Water load tests before and during treatment showed that chlorpropamide, singly and in combination, markedly decreased maximal urinary flow, maximal CH2O, percentage water load excreted, and increased minimal Uosm; clofibrate significantly decreased maximal urinary flow and CH2O only. One patient responded only to combination therapy. Chlorporpamide caused serious hypoglycemia in three of six patients. Clofibrate had no significant side effects.
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PMID:Comparison of clofibrate and chlorpropamide in vasopressin-responsive diabetes insipidus. 86 82

A patient with an enlarged, asymmetric sella turcica and visual field defects suggestive of a pituitary or parasellar tumor underwent extensive roentgenographic and pituitary function studies. No abnormalities in pituitary luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, ACTH, prolactin or vasopressin secretion were detected. Growth hormone secretion was provoked by arginine infusion but not by hypoglycemia. Pneumoencephalography revealed air in the sella turcica, and no evidence of tumor. Thus, an enlarged sella turcica in a patient with visual field defects but normal pituitary function may suggest the presence of an "empty sella syndrome."
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PMID:Primary empty sella syndrome with visual field defects. 93 63

Twelve patients (10 women and 2 men) with a primary empty sella turcica were studied. Endocrine function tests were performed as follows: growth hormone (GH) was measured after insulin-induced-hypoglycaemia, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) after LH-releasing hormone, thyrotrophin (TSH) and prolactin after thyrotrophin-releasing hormone; pituitary reserve of adrenocorticotrophin (ACTH) was determined by measurement of plasma cortisol after lysine-vasopressin and 11 deoxycortisol after metyrapone. Five of the patients (group A) had no endocrine disturbance. Seven patients (group B) had a hypothalamo-pituitary disorder. Two of them had panhypopituitarism which appeared in one case after meningoencephalitis and in the other after a severe cranial trauma. In two cases an amenorrhoea-galactorrhoea syndrome with increased prolactin level (68 and 230 ng/ml) led to a diagnosis of a prolactin producing adenoma, which was confirmed by surgery. Finally three cases of amenorrhoeagalactorrhoea, with normal prolactin level, and/or diabetes insipidus remained unexplained. However, no causal relationship could be demonstrated between the pituitary disturbance and the "empty sella". Primary empty sella turcica is therefore a neuroanatomical and neuroradiological entity with no endocrine implication. A pituitary disorder might suggest a microadenoma or an incidentally associated disease.
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PMID:The primary empty sella an endocrine study on 12 cases. 98 92

Eighteen female rhesus monkeys subjected to complete or anterior disconnection of the medial basal hypothalamus (MBH) were studied to assess the effects of these deafferentation procedures on GH and cortisol secretion. Basal serum levels of GH were not disturbed or were slightly elevated following complete or anterior MBH disconnection. GH secretion in response to vasopressin administration or insulin hypoglycemia, however, was abolished by complete isolation of the MBH. In contrast, the elevations in serum cortisol concentrations observed in response to these noxious stimuli were not noticeably affected. The normal diurnal rhythm in cortisol secretion remained fully evident following anterior deafferentation, but was severely attenuated or abolished when all neuronal inputs to the MBH were transected. Such observations suggest that the central components of the neuroendocrine systems which regulate basal GH secretion and which subserve stress-induced elevations in cortisol secretion are resident within the MBH-hypophysial unit. In addition, these data indicate that the mechanisms underlying the diurnal rhythm in cortisol secretion, as well as those mediating the discharges of GH in response to vasopressin administration and insulin hypoglycemia, are dependent on the integrity of neuronal connections between the MBH and other hypothalamic and/or extrahypothalamic areas.
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PMID:Surgical disconnection of the medial basal hypothalamus and pituitary function in the rhesus monkey. II. GH and cortisol secretion. 116 27


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