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)

1. The fluid sacs and bladders of ten foetuses and the allantoic sacs of five foetuses were catheterized between 79 and 96 days gestational age and daily samples were withdrawn until lambs were born naturally at approximately 147 days. Maternal jugular plasma obtained daily allowed the nutritional status of each ewe to be regulated and monitored. All lambs were observed for 7 weeks, and at post-mortem no abnormalities were seen in those operated upon in utero.2. The osmolality, [Na(+)], [K(+)], [Cl(-)], [glucose], [fructose], [urea], [amino acid] and pH of all samples were measured.3. Foetal surgery seemed to affect the actual concentrations of some solutes, but gestational trends in foetal fluid composition were unaltered.4. Until about 7 days before birth the foetal urine osmolality, [Na(+)], [Cl(-)] and [fructose] decreased, its [urea], [amino acid] and pH remained relatively constant, and from about 120 days gestational age the [K(+)] increased. During the last 7 days there was a marked increase in the osmolality and the concentrations of all these solutes, and a decrease in pH.5. Entry of foetal urine into the fluid sacs tended to decrease the osmolality, [Na(+)], [K(+)], [Cl(-)] and [glucose] of both foetal fluids and the [amino acid] of allantoic fluid, and tended to increase the [fructose] and [urea] of both fluids and the [amino acid] of amniotic fluid.6. Changes in urine composition suggested large daily variations in the secretion of foetal antidiuretic hormone and also a rapid increase in its secretion during the last 7 days, and particularly the last 2-4 days before birth.7. Changes in the [Na(+)]/[K(+)] ratios of foetal urine and allantoic fluid were parallel during post-operative recovery, during the course of pregnancy and immediately before birth, and this was consistent with a simultaneous action of foetal plasma corticosteroids on the foetal kidneys and chorioallantois.8. Variations in the [fructose] of foetal urine and allantoic fluid were parallel to changes in their [Na(+)]/[K(+)] ratios and suggested an involvement of foetal corticosteroids in the regulation of the [fructose] of foetal plasma.9. Further evidence has been presented supporting the hypothesis that maternal induced foetal hypoglycaemia effects a relative increase in the secretion of foetal corticosteroids having an action on the chorioallantois. Also, high concentrations of maternal plasma corticosteroids may decrease the permeability of the placenta to glucose.
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PMID:Daily changes in foetal urine and relationships with amniotic and allantoic fluid and maternal plasma during the last two months of pregnancy in conscious, unstressed ewes with chronically implanted catheters. 464 63

Chlorpropamide was found to be an effective antidiuretic agent in vasopressin-sensitive diabetes insipidus. Full clinical use of this action is limited by the frequent occurrence of hypoglycemia on higher doses. This complication can be avoided, however, by restricting the dose and by employing combination therapy with hydrochlorothiazide.
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PMID:Oral therapy of diabetes insipidus with chlorpropamide. 556 15

The first half of this manuscript is devoted to a review of the methods used and the results obtained in the published measurements of the normal responses to tests of the three main types of hypothalamic-pituitary-adrenocortical (HPA) activity in man. These are, I, basal, unstressed activity leading to appropriate levels of total daily production of cortisol in the characteristic circadian pattern; II, responses to feedback stimulation of HPA activity by metyrapone administration; and III, responses to tests of the effects of stress on the HPA system including the effects of hypoglycemia, induced fever, vasopressin administration, and ACTH injections and infusions. The advantages and shortcomings of each type of procedure are discussed. The second half of this paper describes the authors' attempts to establish the limits of normality of standard and modified methods of evaluating the HPA system. The defined limits of normality have been used to assess the HPA function in 158 patients with known or suspected disorders of the HPA system. In normal controls, halfhourly plasma cortisol determinations established the normality of circadian and postprandial fluctuations and of mean plasma cortisol concentration, 6.2 +/- 0.3 (SEM) micrograms/dl, which were closely approximated by determinations every 6 h. Metyrapone, given in a dose of 500 mg every 2 h for 24 h increased urinary 17-OHCS excretion to 10.5-32.6 mg/day or to 1.7-7.8 times basal excretion rate. Increasing rates of insulin infusion disclosed significant relationships between resulting plasma glucose and cortisol concentrations. The slopes of the delta cortisol/delta glucose responses were similar after insulin infusions (0.46 +/- 0.05) and after insulin injections, 0.15 U/kg (0.43 +/- 0.09), and were always greater than 0.20 micrograms/mg. This index provides a useful objective measure of the normality of responses to hypoglycemic stress, 0.20-0.87 micrograms/mg. Adrenocortical responses to iv infusions of ACTH (cosyntropin 0.25 mg) may be equivocal at 2 h but are clear cut at 4, 6 and 8 h. Of 158 patients in whom hypopituitarism was known or suspected because of the presence of a pituitary tumor, acromegaly, hyperprolactinemia, or clinical features, HPA function was found to be entirely normal in 88 patients and partially or severely abnormal in the remaining 70 patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Normal and abnormal function of the hypothalamic-pituitary-adrenocortical system in man. 608 18

A 28 year old woman presented with symptoms and biochemical findings suggesting hypoglycemia. Detailed endocrine investigations indicated secondary adrenocortical insufficiency with no rise in plasma ACTH or plasma cortisol following insulin-induced hypoglycemia or vasopressin infusion. The adrenal glands however produced cortisol normally following prolonged stimulation with depot tetracosactrin. Other anterior pituitary hormones were released normally following appropriate stimulation tests. The literature on isolated ACTH deficiency is briefly reviewed, and this case represents one of the few reports in which the diagnosis has been substantiated by ACTH radioimmunoassays.
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PMID:Isolated ACTH deficiency confirmed by ACTH radioimmunoassay. 624 62

A complete endocrinological exploration was performed in a 23 year old male patient who presented clinical signs of an acquired panhypopituitarism which appeared two months after a severe head trauma, in order to determine whether the deficit lay in the hypothalamus or in the pituitary. TSH had normal basal levels, but presented a delayed rise after TRH administration. PRL rose normally after TRH administration, but presented a blunted response to both metoclopramide and insulin tolerance test. Cortisol rose significatively after lysine vasopressin, but failed to rise during insulin hypoglycaemia. These results are consistent with a hypothalamic defect. Extensive endocrinological data are often lacking in the few similar cases reported in the literature. Prl and TSH were usually found to have normal basal levels while other pituitary hormones were profoundly lowered. This was interpretated as a pituitary defect with some intact areas of the anterior lobe. However, this may also suggest a hypothalamic defect which could have been assessed by mor discriminative tests.
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PMID:Panhypopituitarism secondary to head trauma: evidence for a hypothalamic origin of the deficit. 624 99

Using a specific radioimmunoassay for gamma-melanotropin (gamma-MSH), one of the predicted fragments in the amino-terminal portion of the adrenocorticotropin(ACTH)-beta-lipotropin (beta-LPH) precursor, gamma-MSH-like immunoreactivity (gamma-MSH-LI) was detected in human plasma from 4 of 5 patients with Addison's disease and 2 of 3 patients with Nelson's syndrome. None of the normal subjects or patients with Cushing's disease showed detectable concentrations (more than 150 pg/ml) of gamma-MSH-LI. gamma-MSH-LI was secreted concomitantly with ACTH-like immunoreactivity (ACTH-LI) and beta-endorphin-like immunoreactivity (beta-endorphin-LI) in response to insulin-induced hypoglycemia and the administration of lysine-vasopressin. Conversely, intravenous injection of cortisol lowered plasma concentrations of gamma-MSH-LI concomitantly with those of ACTH-LI and beta-endorphin-LI. Gel chromatographic studies of the plasma extracts showed a single peak of gamma-MSH-LI near the elution position of human beta-LPH. These results suggest that gamma-MSH-LI in human plasma is present as a big form and that this big gamma-MSH is secreted concomitantly with ACTH and beta-endorphin.
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PMID:Concomitant secretion of Y-MSH with ACTH and beta-endorphin in humans. 625 36

Deficiencies of corticotrophin (ACTH), growth hormone, and prolactin were documented in a woman with diabetes mellitus and Sheehan's syndrome. The patient's ACTH deficit appeared to be secondary to a hypothalamic abnormality since on two occasions the patient had a marked plasma ACTH response to vasopressin but not to insulin induced hypoglycaemia. It is postulated that the deficits of these three adenohypophysial hormones were instrumental in causing a severely impaired aldosterone secretory capacity in response to sodium restriction and an angiotensin infusion. In addition, the patient had an unusual form of thyroid dysfunction that was in part reversed with hydrocortisone replacement. The patient's unfortunate death during a hypoglycaemic crisis allowed correlation between her extensive antemortum endocrine testing and her pathologic anatomy.
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PMID:Corticotrophin, growth hormone and prolactin deficiencies with hypoaldosteronism and corticosteroid-reversible hypothyroidism in Sheehan's syndrome. Clinical and anatomical correlations. 625 5

The primary site of action of insulin hypoglycemia to induce ACTH secretion was investigated in rats with medial basal hypothalamic ablation (MBHA), medial basal hypothalamic deafferentation (MBHD), and chlorpromazine-morphine-pentobarbital (C-M-P) treatment. Plasma corticosterone (B) concentration was used as an index of ACTH secretion. Hypoglycemia failed to provoke ACTH secretion in MBHA and C-M-P treated animals, while it stimulated ACTH secretion in MBHD animals to the same extent as in controls. The rise in plasma B induced by synthetic lysine-vasopressin injection was not significantly different between MBHA and control animals, indicating pituitary ACTH reserve was not affected by the operation. Our data indicate that hypoglycemia stimulates ACTH secretion through a primary effect in the medial basal hypothalamus and not in the extrahypothalamic CNS or adenohyphophysis.
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PMID:Hypoglycemia stimulates ACTH secretion through a direct effect on the basal hypothalamus. 626 29

An 8-yr-old girl is presented who had periodic attacks of vomiting, psychotic depression, drowsiness, and hypertension (160/110 mm Hg) for a period of 16 months after head injury. At the initiation of the attack, serum ACTH and vasopressin levels were prominently increased (610 pg/ml and 41 microunits/ml, respectively), followed by hypercortisolemia, hyponatremia, and hypoosmolality in plasma. Serum PRL also was elevated (91 ng/ml). Responses of GH and cortisol to insulin-induced hypoglycemia and those of TSH to TRH were reduced. Urinary excretion of epinephrine and norepinephrine were increased, while dopamine (DA) excretion was reciprocally decreased, resulting in a marked elevation of the epinephrine plus norepinephrine to DA ratio during the episodes (0.4-4.5); this was normalized on attack-free days (0.08-0.25). During the attack, the concentration of homovanillic acid, a major metabolite of DA in the brain, also was reduced in cerebrospinal fluids from 70 to 23 ng/ml. The administration of methyl-dopa and reserpine effectively suppressed the recurrence of the episode. Although the exact cause of this syndrome is unknown, a periodic metabolic dysfunction of catecholamine in the central nervous system might be postulated.
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PMID:A syndrome of periodic adrenocorticotropin and vasopressin discharge. 627 29

Anterolateral hypothalamic deafferentiation was made in rats to explore the importance of the neural pathways through the lateral retrochiasmatic area (RCAL) in the regulation of ACTH and TSH secretion. In rats with complete bilateral RCAL transection, pituitary-adrenal function was altered in the following respects compared to sham-operated controls. 1) Basal plasma ACTH, corticosterone (B), and adrenal weight were depressed. 2) Plasma ACTH and B elevation in response to 3-min ether inhalation were markedly decreased or abolished. 3) Insulin-induced hypoglycemia produced no or little plasma B elevation. 4) Lysine-vasopressin was significantly less effective in inducing pituitary-adrenal activation. Reductions in plasma ACTH and B concentrations and adrenal weight were correlated with the completeness of the RCAL transection. The plasma TSH concentration was lower in the deafferented rats than in the controls regardless of the completeness of the cut at the RCAL, indicating that the neural pathways traversing this area do not possess a critical importance for the regulation of TSH if the rest of the hypothalamus is deafferented anterolaterally. We conclude that intact neural connections between the medial basal hypothalamus and the central nervous system at the RCAL are essential for the maintenance of normal hypothalamic-pituitary-adrenal function.
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PMID:The importance of the hypothalamic lateral retrochiasmatic area in the control of adrenocorticotropin and thyrotropin secretion. 628 Sep 72


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