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)

Pituitary apoplexy is a neuroendocrine emergency produced by hemorrhage or infarction of pituitary tumors, and its accurate diagnosis has relied mainly on clinical manifestations and computed tomography (CT) scan of sella in the past. A case is reported of pituitary apoplexy which was demonstrated on magnetic resonance imaging (MRI). The 72-year-old male patient was admitted to the Nephrology Section of VGH-Taipei with symptoms of general malaise, poor appetite for four months and apparent hyponatremia (Na 102 mEq/L) on laboratory findings. Under the impression of syndrome of inappropriate secretion of antidiuretic hormone (SIADH), fluid restriction and infusion of isotonic saline were prescribed, but in vain. The patient was transferred to the Endocrinology Section because of lowered serum cortisol, T3, T4, and hs-TSH levels. Dynamic pituitary function tests confirmed the diagnosis of panhypopituitarism. Contrast enhanced CT scan of sella revealed displacement of the pituitary stalk to the right side. T1-weighted MRI showed persistent high intensity in left sella and T2-weighted MRI showed persisting isointense to white matter. The hyponatremia and clinical symptoms resolved within a few days after replacement therapy with glucocorticoid and thyroid hormone. It was concluded that MRI is more sensitive than CT scan for detecting subacute or chronic pituitary apoplexy.
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PMID:Pituitary apoplexy diagnosed by magnetic resonance imaging: a case report. 775 60

The potential efficacy of early repeat transsphenoidal surgery for persistent Cushing's disease has not previously been examined. On 222 patients with no prior pituitary treatment and a preoperative diagnosis of Cushing's disease, 29 (13%) remained hypercortisolemic after an initial transsphenoidal pituitary exploration. Seventeen of these 29 patients underwent further surgery 7 to 46 days after the initial transsphenoidal approach in order to completely excise suspected residual tumor. Patients were followed for 4 to 84 months (mean +/- standard deviation, 34 +/- 25 months) to document sustained remission or recurrence of Cushing's disease (a urine free cortisol level > 90 micrograms/day was considered evidence of recurrence). Of the 17 patients with repeat surgery, 12 (71%) had resolution of hypercortisolism (morning plasma cortisol level < 5 micrograms/dl); however, in three of these 12, hypercortisolism recurred 5, 12, and 24 months later. In 14 patients a lesion that appeared to be a tumor was identified during the initial procedure or on histological examination. Of these, 12 had immediate resolution of hypercortisolism and nine are still in remission. Three patients, in whom no adenoma could be identified during the initial surgery or an examination of the partial hypophysectomy specimen from the initial surgery, had persistent Cushing's syndrome after the second operation. Seven (41%) of the 17 patients developed hypopituitarism requiring treatment with thyroid hormone, gonadal steroid, or vasopressin replacement. The low incidence of identification of an adenoma on computerized tomography or magnetic resonance images (three of 17 patients), the failure to find a corticotrophic adenoma during the initial surgery (10 of 17 patients), and the failure of these 17 patients to respond to the initial transsphenoidal surgery suggest that they may comprise a subset of patients who are more difficult to treat successfully with surgery than most patients with Cushing's disease. Despite that, early reoperation induced immediate remission of hypercortisolism in 71% of cases, but did so at the expense of a high risk of hypopituitarism. However, since the alternative treatments (such as radiation therapy, long-term drug therapy, or bilateral adrenalectomy) also have potential adverse effects, early reoperation deserves consideration for the management of persistent Cushing's disease, especially when an adrenocorticotrophic hormone-secreting adenoma was partially excised during the first surgery.
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PMID:Early repeat surgery for persistent Cushing's disease. 827 Oct 20

The survival rate of patients undergoing cardiopulmonary resuscitation (CPR) is 5% to 15%. New treatment approaches under investigation for CPR include the use of vasopressin as a vasopressor, amiodarone for the treatment of ventricular tachyarrhythmia, and adenosine antagonists (i.e., theophylline) for bradyasystolic rhythms. More innovative approaches include the use of thyroid hormone and endothelin.
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PMID:Innovative pharmacologic approaches to cardiopulmonary resuscitation. 975 3

The atrial natriuretic hormone (ANP) is a cardiac hormone which gene and receptors are widely present in the body. Its main function is to lower blood pressure and to control electrolyte homeostasis. Its main targets are the kidney and the cardiovascular system but ANP interacts with many other hormones in order to regulate their secretion. The adrenal glands are the first endocrine target. Steroidogenesis, especially mineralocorticoid synthesis, is inhibited by ANP, but glucocorticoid production seems to be depressed too. As ANP synthesis is enhanced by the latter, it suggests a regulatory loop. Moreover ANP inhibits the thyroid synthesis whereas its production is enhanced by thyroid hormone. The hypothalamo-hypophyseal axis is another important target. ANP inhibits ACTH release and arginine vasopressin secretion. Vasopressin enhances ANP synthesis while GH decreases it. Finally the endocrine effects of ANP strengthen the cardiovascular and renal effects of the hormone, antagonizing the salt and water retention due to aldosterone and AVP. Because of a local production, ANP may also act as a paracrine hormone that influences the function of many endocrine systems (ovarian function for instance). In the central nervous system, ANP acts as a neurotransmitter in order to regulate pituitary and vegetative functions. Plasma ANP levels are impaired in several endocrine diseases : the plasma hormone levels increase in hypercortisolism, hyperaldosteronism, thyrotoxicosis and inappropriate antidiuretic hormone secretion; it decreases in hypothyroidism. In case of Addison's disease, ANP may be used to assess the quality of mineralocorticoid treatment, in association with the other biological criteria.
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PMID:[Atrial natriuretic hormone and endocrine functions]. 1021 Jul 41

A 60-year-old woman was admitted with severe hyponatremia. Basal values of adrenocorticotropic hormone (ACTH), thyroid hormone and cortisol were normal on admission. Impairment of water diuresis was observed by water loading test. Initially, we diagnosed her condition as the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). By provocation test, we finally confirmed that the hyponatremia was caused by hypothalamic adrenal insufficiency. The basal values of ACTH and cortisol might not be sufficient to exclude the possibility of adrenal insufficiency. Therefore, it is necessary to evaluate adrenal function by provocation test or to re-evaluate it after recovery from hyponatremia.
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PMID:Severe hyponatremia caused by hypothalamic adrenal insufficiency. 1039 72

Glucagon-like peptide-1 (GLP-1), a potent regulator of glucose homeostasis, is also produced in the central nervous system, where GLP-1 has been implicated in the neuroendocrine control of hypothalamic-pituitary function, food intake, and the response to stress. The finding that intracerebroventricular GLP-1 stimulates LH, TSH, corticosterone, and vasopressin secretion in rats prompted us to assess the neuroendocrine consequences of disrupting GLP-1 signaling in mice in vivo. Male GLP-1 receptor knockout (GLP-1R-/-) mice exhibit reduced gonadal weights, and females exhibit a slight delay in the onset of puberty; however, male and female GLP-1R-/- animals reproduce successfully and respond appropriately to fluid restriction. Although adrenal weights are reduced in GLP-1R-/- mice, hypothalamic CRH gene expression and circulating levels of corticosterone, thyroid hormone, testosterone, estradiol, and progesterone are normal in the absence of GLP-1R-/- signaling. Intriguingly, GLP-1R-/- mice exhibit paradoxically increased corticosterone responses to stress as well as abnormal responses to acoustic startle that are corrected by glucocorticoid treatment. These findings suggest that although GLP-1R signaling is not essential for development and basal function of the murine hypothalamic-pituitary-adrenal axis, abrogation of GLP-1 signaling is associated with impairment of the behavioral and neuroendocrine responses to stress.
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PMID:Neuroendocrine function and response to stress in mice with complete disruption of glucagon-like peptide-1 receptor signaling. 1065 Sep 25

We have investigated with histochemical techniques the expression of peptides and other neurochemical markers in the hypothalamus and olfactory bulb of male mice, in which the genes encoding the alpha and beta thyroid hormone receptors (TRalpha1, TRbeta1 and TRbeta2) have been deleted. Thyrotropin-releasing hormone messenger RNA levels were increased in the hypothalamic paraventricular nucleus and in the medullary raphe nuclei of mutant mice lacking the thyroid hormone receptors alpha1 and beta (alpha1(-/-)beta(-/-)), as compared to wild-type mice. In contrast, galanin messenger RNA levels were lower in the hypothalamic paraventricular nucleus of mutant animals, as was galanin-like immunoreactivity in the internal layer of the median eminence. Substance P messenger RNA levels were unchanged in the medullary raphe nuclei. Thyrotropin-releasing hormone receptor messenger RNA levels were increased in motoneurons, unchanged in the subiculum, and lower in the amygdala of mutant animals. Galanin messenger RNA levels were unchanged in the hypothalamic dorsomedial and arcuate nuclei of the thyroid hormone receptor alpha1(-/-)beta(-/-) mice, as was the immunocytochemistry for oxytocin and for vasopressin in the hypothalamic paraventricular nucleus. A reduction in tyrosine hydroxylase messenger RNA levels was found in the arcuate nucleus of mutant mice. In the olfactory bulb, immunohistochemistry for calbindin and for tyrosine hydroxylase revealed a reduction in the intensity of labeling of nerve processes in the glomerular layer of thyroid hormone receptor alpha1(-/-)beta(-/-) mice. The tyrosine hydroxylase messenger RNA levels were also slightly reduced. In contrast, the levels of galanin and neuropeptide Y messenger RNA in this region were unchanged in thyroid hormone receptor alpha1(-/-)beta(-/-) mice as compared to wild-type mice. Together these studies reveal many regional and neurochemically selective alterations in neuronal phenotype of mice devoid of all known thyroid hormone receptors.
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PMID:Expression of peptides and other neurochemical markers in hypothalamus and olfactory bulb of mice devoid of all known thyroid hormone receptors. 1111 49

We report a 70-year-old woman with hypothyroidism and severe hyponatremia. Her plasma antidiuretic hormone (ADH) level was inappropriately high for her low plasma osmolality. Her low serum sodium level was gradually corrected by water restriction and sodium supplementation prior to the initiation of thyroid hormone replacement. After a diagnosis of Hashimoto's thyroiditis had been made, the patient was treated with levothyroxine. Following this treatment, the patient's serum sodium level increased drastically. It is suggested that the elevated plasma ADH level played an important role in the development of hyponatremia in this case.
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PMID:Hyponatremia with increased plasma antidiuretic hormone in a case of hypothyroidism. 1119 79

Hyponatremia is a common disorder. When hyponatremia is the result of hypothyroidism it can be successfully treated with thyroid hormone substitution. We followed cumulative sodium- and fluid balances of a patient with hyponatremia, resulting from hypothyroidism. We concluded that hyponatremia in hypothyroidism is due to a pure renal mechanism, and cannot be ascribed to inappropriate secretion of antidiuretic hormone.
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PMID:Hyponatremia due to hypothyroidism: a pure renal mechanism. 1124 14

More efficient and faster separation conditions for qualitative as well as quantitative analysis of neuropeptides in human plasma using capillary zone electrophoresis (CZE) have been developed. The analysis method for neuropeptides has been improved specifically to study thyroid hormone related neuropetides for the regulation of thyroid disease. In this study, we investigated the pretreatment methods, composition of the running buffer and rinsing procedures between runs in order to obtain more sensitive and faster separation of trace neuropeptides in plasma by CZE. The tested neuropeptides were somatostatin (SOMA), vasopressin (VP), neurotensin (NT), and thyrotropin-releasing hormone (TRH). Plasma samples were pretreated by deproteinization and solid-phase extraction method. The fraction of neuropeptides was reconstituted in 40% acetonitrile followed by ultrafiltration, and then analyzed by CZE. Resolution and sensitivity was improved using the separation buffer composition with 100 mM Tris-phosphate buffer (pH 2.0) while the sensitivity was further improved via a stacking method using the sample buffer of 40% acetonitrile. These sample pretreatment methods and buffer condition permit quantitative analysis on tested neuropeptides at the 20 ng/mL level. The rinsing procedures between runs using 90% ethanol dramatically shortened the rinsing time to 30 min.
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PMID:Influence of buffer composition and sample pretreatment on efficiency separation for monitoring neuropeptides in plasma using capillary electrophoresis. 1150 49


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