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 establish whether arginine-vasopressin (AVP) release in response to insulin-induced hypoglycemia is mediated by a muscarinic and/or nicotinic cholinergic pathway, 12 normal men had an insulin tolerance test (ITT) in basal conditions and after treatment with the muscarinic receptor blocker pirenzepine (40 mg IV (intravenously) ten minutes before ITT in six subjects) or the nicotinic receptor antagonist trimethaphan (0.3 mg/min X 30 min IV before ITT in six subjects). The drugs did not modify arterial blood pressure nor produce side effects capable of altering AVP secretion. Pirenzepine administration did not change AVP response to hypoglycemia, whereas trimethaphan significantly reduced AVP increase by about 50% during the ITT. These data suggest the involvement of a cholinergic-nicotinic mechanism in regulation of AVP response to hypoglycemia.
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PMID:Nicotinic-cholinergic involvement in arginine-vasopressin response to insulin-induced hypoglycemia in normal men. 352 15

Two adult patients with unilateral hypoplastic optic nerves, absent septa pellucida and hypopituitarism are described. Patient 1, aged 20, presented with diabetes insipidus due to partial vasopressin deficiency. Patients 2, aged 29, presented with focal epilepsy. Both had short stature. They showed absent growth hormone (GH) response to insulin-hypoglycaemia or glucagon, but responded to 100 micrograms growth hormone releasing factor (GRF-44) with a rise in circulating GH, suggesting a hypothalamic defect in GH release though a co-existing pituitary defect cannot be excluded. Other hypothalamic-pituitary functions were normal. These two patients probably represent the milder form of the clinical spectrum of septo-optic dysplasia which, with the extensive use of CT brain scans, will be increasingly encountered by physicians attending adult patients.
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PMID:Hypothalamic defects in two adult patients with septo-optic dysplasia. 375 51

We describe a 30 year old man who developed chronic adipsic hypernatraemia and hypothermia following a subarachnoid haemorrhage from an anterior communicating artery aneurysm. Anterior pituitary function tests were normal. Hypothermia was demonstrated over 4 years with loss of the ability to control heat conservation despite body temperatures as low as 30 degrees C. He failed to experience thirst despite plasma sodium concentrations of up to 187 nmol/l and plasma osmolalities of up to 397 mOsm/kg. The slope of the plasma vasopressin-plasma osmolality curve indicated loss of the osmoreceptor. There was an absent vasopressin response to insulin-induced hypoglycaemia but a normal response to apomorphine. The apomorphine-stimulated immunoreactive vasopressin was shown to behave identically to the synthetic peptide on HPLC and was bioactive.
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PMID:Chronic hypernatraemia and hypothermia following subarachnoid haemorrhage. 377 77

Release of human neurophysin I (hNp I) and neurophysin II (hNp II) during insulin-induced hypoglycemia was studied in 10 unipolar depressed women before and after 4-5 weeks of standard antidepressant drug treatment with daily intravenous infusions of clomipramine. Before treatment, a significant increase of hNp I but not of hNp II serum levels in response to hypoglycemia was observed. At retest during clomipramine administration, a marked clinical amelioration occurred in all patients as determined with the Hamilton Rating Scale for Depression; the hNp I response to insulin was abolished, but no effect on hNp II concentration could be demonstrated. No correlation was found between the degree of the depression score decrease and the amplitude of the inhibition of hNp I release or serum levels of clomipramine or its metabolite, desmethylclomipramine. The meaning of this difference in reactivity of the neurohypophyseal system in the course of depressive illness, based on the pharmacological and biochemical profiles of clomipramine action, is discussed.
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PMID:Release of human neurophysin I during insulin-induced hypoglycemia in depressed patients is abolished after recovery with clomipramine treatment. 388 65

We describe a 24-year-old short, obese girl who has bizarre episodic neurological abnormalities related to hyperosmolality due to hypernatraemia. Investigation of osmoregulation by water loading and infusion of hypertonic saline revealed (i) hypodipsia with thirst onset raised to plasma osmolality of 332 mmol/kg and (ii) elevation of the threshold for vasopressin release (plasma osmolality 320 mmol/kg) but normal slope of the plasma vasopressin-plasma osmolality curve. Baroregulated vasopressin release was also grossly subnormal. Other hypothalamo-pituitary investigations showed deficiencies of releasing hormones for gonadotrophins and growth hormone, but prolactin response to combined hypoglycaemia and TRH was blunted She demonstrated other anomalies including hyperlipoproteinaemia and defective lymph drainage of the legs. Skull X-rays, together with computerized tomography and nuclear magnetic resonance scans of the hypothalamo-pituitary region and the rest of the brain were normal. We believe that this is the first case of essential hypernatraemia documented with direct evidence of resetting of the osmostat.
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PMID:A case of 'essential' hypernatraemia due to resetting of the osmostat. 398 72

We report an 18-month-old girl with Cushing's disease caused by a large adenoma of the pituitary gland. Tumour size and extension were determined by X-ray, CT-scan and angiographic studies. The endocrinological findings were typical for this disease: elevated plasma levels of ACTH, cortisol, 17-Hydroxyprogesterone (17-OHP) and testosterone, elevated urinary excretion of 17-Ketosteroids (17-KS) and 17-Hydroxycorticoids (17-OHCS). Dexamethasone failed to suppress ACTH and cortisol plasma levels. TRH induced only a minimal TSH increase. Following LH-RH injection gonadotropin levels rose to pubertal values. The hGH response to insulin-induced hypoglycaemia was subnormal. After resection of the tumour the infant died because of non-treatable arrhythmia. Histological findings showed a non-differentiated adenoma with extension into the subarachnoid space and into nerve tissues. In vitro lysine-vasopressin (LVP) and arginine-vasopressin (AVP) exhibited only weak stimulatory effects on the ACTH secretion of the tumour cells.
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PMID:Cushing's disease due to an unusually large adenoma of the pituitary gland in infancy. 398 21

Techniques are described in detail for a radioimmunoassay of plasma adrenocorticotropin (ACTH) that is capable of detecting hormone in unextracted normal human plasma at 1:5 dilution under the conditions described. The sensitivity of the assay is at the level of 1 mumug/ml (equivalent to 0.014 mU/100 ml). In normal subjects ACTH concentrations averaged 22 mumug/ml (equivalent to 0.308 mU/100 ml) plasma at 8-10 a.m. In a smaller group the concentrations averaged 9.6 mumug/ml (equivalent to 0.134 mU/100 ml) at 10-11 p.m. Although a circadian rhythm in normal subjects was not always well marked throughout the daytime hours, plasma ACTH usually fell to its lowest value in the late evening. In hospital patients who were not acutely ill, concentrations were infrequently above 100 mumug/ml in the morning and usually fell to significantly lower levels in the late evening. Severely ill hospital patients occasionally exhibited a.m. concentrations above 200 mumug/ml. In a group of subjects showing frequent spiking of plasma 17-OHCS concentrations throughout the day parallel spiking of plasma ACTH as well was generally observed.Metyrapone produced marked increases in plasma ACTH within 24 hr in all cases and generally within 3-6 hr except when started late in the day. Dexamethasone brought about a persistent reduction in plasma ACTH in a patient under continued treatment with metyrapone.Hypoglycemia, electroshock, surgery under general anesthesia, histalog and vasopressin administration were usually followed by significant increases in plasma ACTH concentration. Prior administration of dexamethasone blocked the response to hypoglycemia. Marked elevations in plasma ACTH were observed in patients with adrenal insufficiency off steroid therapy, in Cushing's disease after adrenalectomy even in the presence of persistent hypercortisolemia, and in some untreated patients with Cushing's disease. Umbilical cord blood contained higher plasma ACTH concentrations than maternal blood at delivery in seven of eight cases. After suppression of ACTH secretion by dexamethasone or cortisol. ACTH disappeared from plasma with half-times ranging from 22 min to 30 min in three cases studied.
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PMID:Radioimmunoassay of ACTH in plasma. 430 80

Four patients treated with depot tetracosactrin for 10 to 18 months maintained normal hypothalamic-pituitary-adrenal function assessed by the nyctohemeral variation of plasma corticosteroids and by the responses of plasma corticosteroids to insulin-induced hypoglycaemia, lysine-vasopressin, and depot tetracosactrin. The pituitary component of the response was analysed by measuring plasma immunoreactive ACTH levels. Three patients showed a nyctohemeral ACTH rhythm and normal ACTH responses to insulin-induced hypoglycaemia. Consistently undetectable morning plasma ACTH levels were found in the fourth patient, who also showed an unusually delayed rise in both ACTH and corticosteroid levels in response to insulin-induced hypoglycaemia, though the peak values attained were normal.The lack of suppression of hypothalamic-pituitary-adrenal function together with the good clinical response in these four patients suggests that treatment with depot tetracosactrin should be considered when long-term corticosteroid therapy is required.
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PMID:Hypothalamic-pituitary-adrenal function in patients treated with long-term depot tetracosactrin. 432 39

Plasma corticotrophin (ACTH) and corticosteroid levels in response to lysine vasopressin (LVP), insulin hypoglycaemia, and pyrogen have been compared in seven subjects with normal pituitary adrenal function. Intramuscular vasopressin was a weak stimulus to corticotrophin release, peak values lying within the range 49 to 141 pg/ml. Insulin hypoglycaemia consistently caused a more noticeable increase, with peak levels between 114 and 364 pg/ml, while pyrogen was the most powerful, corticotrophin levels rising to between 209 and 1,725 pg/ml. Peak plasma corticosteroid levels showed less pronounced differences between the three tests, and correlated poorly with peak ACTH levels. Thus, relatively small acute changes in corticotrophin levels produce near-maximal adrenal stimulation. Under these conditions, plasma corticosteroid measurements do not accurately reflect circulating corticotrophin levels. These findings help to explain the physiological basis of several observations on the corticosteroid responses to these clinical test procedures.
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PMID:Comparison of corticotrophin and corticosteroid response to lysine vasopressin, insulin, and pyrogen in man. 434 79

A 29-year-old woman with evidence of a craniopharyngioma and documented panhypopituitarism is described. Clinical and laboratory evaluation revealed deficiencies of follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, growth hormone, prolactin, adrenocorticotropic hormone and antidiuretic hormone. Prompt release of several pituitary hormones was noticed after administration of the hypothalamic releasing hormones FSH/LH-RF and thyrotropin-releasing hormone, whereas insulin-induced hypoglycemia, levodopa, chlorpromazine and clomiphene citrate, all of which act at the level of the hypothalamus, did not alter basal pituitary secretion. The patient's height of 60 inches, despite panhypopituitarism, and the interpretation of the above data are discussed in the light of current concepts regarding the dynamics of the hypothalamic-hypophyseal system.
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PMID:Survival and growth in a woman with untreated hypothalamic panhypopituitarism of 21 years' duration. 437 Apr 18


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