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)

Sixty children with acute bacterial meningitis (ABM) were prospectively studied for their serum sodium values and cerebrospinal fluid (CSF), serum and urinary osmolality. The results have been compared with 20 age and nutritionally matched controls. Even though mean serum osmolality (283.2 +/- 13.84 mOsm/kg) and serum sodium levels (130.5 +/- 8.15 mEq/L) were significantly lower in ABM in comparison to controls (p < 0.05 and < 0.001, respectively), the overall mean CSF osmolality in patients with ABM (282.5 +/- 12.3 mOsm/kg) was not significantly different as compared to controls (288.2 +/- 7.89 mOsm/kg). As expected, cases of ABM with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) had significantly lower CSF osmolality (272 +/- 9.42 mOsm/kg) as compared to those without SIADH (288.5 +/- 9.34 mOsm/kg) and controls (288.2 +/- 7.89 mOsm/kg). However, our observations indicate that whereas the mean CSF osmolality was lower than the serum osmolality in the control group as well as in ABM without SIADH, it was greater than serum osmolality in ABM with SIADH (p < 0.05). Our results suggest that in the presence of SIADH, hypo-osmolality of serum may eventually result in hypo-osmolality of CSF, but the fall in CSF osmolality is not of the same degree as that of serum. Low CSF osmolality was observed to be associated with an unfavorable prognosis (p < 0.05).
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PMID:Cerebrospinal fluid osmolal changes in bacterial meningitis. 807 10

Rats were exposed to osmotic stress either acutely, over periods of 1 or 4 h, or chronically, over several days. In acute experiments, hyposmolality was induced by intraperitoneal infusion of dilute glucose or mannitol solutions, whereas hyperosmolality was induced by use of sodium chloride, concentrated glucose or mannitol solutions, or urea. Chronic hypernatremia was induced by daily administration of sodium chloride to water-deprived animals; chronic hyponatremia was induced by daily injection of antidiuretic hormone supplemented with glucose. Animals were made hyperglycemic using streptozotocin or uremic by ureteral ligation. Where appropriate, animals were anesthetized with thiobutabarbital (Inaktin) or ether. In acute experiments, analysis of the composition of the cardiac ventricle, diaphragm, liver, and renal cortex showed no evidence of cell volume regulatory processes involving transmembrane movement of potassium ions. There was a small but significant increase in free amino acids [measured as ninhydrin-positive substance (NPS)] in cardiac muscle exposed to hypertonic solutions of sodium chloride and glucose but not when plasma osmolality was raised using mannitol. In cerebral cortical tissue, after 4 h of exposure to acute hypertonicity by infusion of sodium chloride or glucose, there was a significant increase in tissue potassium content and a slight increase in NPS content. In chronic experiments, tissue analysis revealed good evidence for cellular volume readjustment only in cerebral cortex and heart. In the cortex, levels of free amino acids, principally taurine and glutamate (plus glutamine), showed large increases during hypernatremia and hyperglycemia and corresponding decreases during hyposmolality. In heart the principal amino acid present was taurine, and it, together with aspartate and glutamate (plus glutamine), showed large changes under osmotic stress. Other tissues analyzed showed only small changes in composition.
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PMID:Response of tissues of the rat to anisosmolality in vivo. 832 70

Plasma osmolality normally decreases in early pregnancy, reaching a minimum at approximately 10 weeks and remaining depressed until term. This is associated with a mean decrease of 4 mEq/L in the plasma sodium level, and with an altered threshold for arginine vasopressin (AVP) release and for thirst. We describe a patient who developed more severe hyponatremia (120 mEq/L), which accompanied the development of hypertension and edema at 37 weeks in her fourth pregnancy. Hyponatremia and hypo-osmolality were associated with marked elevation of the plasma AVP level. The hyponatremia and elevated AVP level resolved after the delivery of the infant. To our knowledge, this is the first reported example of transient inappropriate antidiuretic hormone secretion (SIADH) associated with pregnancy.
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PMID:Transient syndrome of inappropriate antidiuretic hormone secretion during pregnancy. 846 26

A case of malignant thymoma with pure red cell aplasia (PRCA) complicated by syndrome of inappropriate secretion of antidiuretic hormone (SIADH) following intrathoracic cisdichlorodiammine platinum (CDDP) administration is reported. A 59-year-old Japanese woman who presented with severe general fatigue was diagnosed with PRCA associated with a thymoma, based on the findings of a bone marrow biopsy, computed tomography of the chest, and the existence of anti-acetylcholine receptor antibodies. She underwent a thymectomy after frequent blood transfusions. This was followed by intrathoracic CDDP administration, because of pleural dissemination. Nine days following chemotherapy, her serum sodium concentration was found to be 104mM, while her consciousness was drowsy with severe fatigue and vomiting. This hyponatremic state was diagnosed as SIADH induced by CDDP infusion into the thoracic space, based on the hypo-osmolality of her serum, the hyper-osmolality of her urine, and an inappropriate level of plasma vasopressin.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone following intra-thoracic cisplatin. 873 84

To assess the action of antidiuretic hormone (ADH) and the osmolality of bathing solution on amiloride-sensitive Na+ transport, we measured the amiloride-sensitive short-circuit current (Isc) and single-channel currents in renal epithelial A6 cells. The A6 cells were cultured on permeable supports for 9-13 d without aldosterone treatment. The basal amiloride-sensitive Isc and the density of the amiloride-sensitive Na+ channel at the apical membrane increased as the osmolality of the bathing solution decreased. ADH stimulated the amiloride-sensitive Isc. The stimulatory action of ADH was enhanced by low osmolality. The stimulatory action of hyposmolality on the amiloride-sensitive Isc was significantly diminished by pretreatment with brefeldin A (BFA, a blocker of protein translocation), while BFA had no significant effect on the ratio of ADH-stimulated amiloride-sensitive Isc to basal amiloride-sensitive Isc. These results suggest that hyposmolality stimulates the translocation of amiloride-sensitive Na+ channels to the apical membrane from the cytosolic store sites of the channel, and that ADH may activate amiloride-sensitive Na+ channels pre-existing in the apical membrane or translocate the channel via BFA-insensitive pathways in a manner dependent on the osmolality of the bathing solution in aldosterone-untreated A6 cells, differently from aldosterone-treated A6 cells in which ADH stimulates the translocation of amiloride-sensitive Na+ channels via BFA-sensitive pathways.
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PMID:Hyposmolality-induced enhancement of ADH action on amiloride-sensitive Isc in renal epithelial A6 cells. 915 52

Hyponatraemia is common among the elderly, and may be caused by physiological changes, disease processes or drugs. About half of elderly patients with hyponatraemia have features typical of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). It is important to establish whether drugs are the cause, as this is easily remediable. The clinical manifestations of SIADH are predominantly attributable to hyponatraemia and serum hypo-osmolality. The severity of the signs and symptoms depends on the degree of hyponatraemia and the rapidity with which the syndrome develops. Although a growing number of drugs have been reported to produce SIADH, most published reports concern vasopressin and its analogues, thiazide and thiazide-like diuretics, chlorpropamide, carbamazepine, antipsychotics, antidepressants and nonsteroidal anti-inflammatory drugs. Old age is a risk factor for SIADH following the use of many of these drugs. The use of these drugs in combination, excessive fluid intake and other underlying conditions that limit free water excretion increase the risk. Drug-induced SIADH usually resolves following cessation of the offending agent(s). Additional measures are required in patients with symptomatic hyponatraemia, including fluid restriction and intravenous sodium chloride and/or furosemide (frusemide) therapy. Careful monitoring is essential, with particular attention paid to the rate and extent of correction of the hyponatraemia.
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PMID:Drug-induced syndrome of inappropriate antidiuretic hormone secretion. Causes, diagnosis and management. 923 39

In a minority of patients with malignant tumors, signs and symptoms develop that cannot be explained on the basis of the mass effect produced by the primary tumor or its metastases, or production of a hormone normally associated with the tissue type that has given rise to the malignant tumor; these peculiar symptom complexes are known as paraneoplastic syndromes, and may be divided into endocrinologic, dermatologic, hematologic, neurologic, and osteoarticular manifestations. In the head and neck region in particular, the syndrome of inappropriate antidiuretic hormone production (SIADH, or Schwartz-Bartter syndrome) is a well-recognized form of paraneoplastic syndrome that may accompany head and neck malignancies. Most of such tumors are squamous carcinomas, with lesser numbers of olfactory neuroblastomas, small cell neuroendocrine carcinomas, adenoid cystic carcinomas, and undifferentiated carcinomas; sarcoma was reported in only a single instance. The lesions associated with the development of SIADH have most often been located in the oral cavity, and less often in the larynx, nasopharynx, hypopharynx, nasal cavity, maxillary sinus, parapharyngeal space, salivary glands, and oropharynx. Key features of SIADH include serum hypo-osmolality; an unexpectedly high urinary specific gravity; an absence of edema or dehydration; normal adrenal, thyroid, and renal function; hyponatremia; and an elevation of plasma vasopressin.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion associated with head neck cancers: review of the literature. 934 88

We here report a case presenting with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after having been treated for pleurodesis with OK-432, which is a lyophilized preparation of an attenuated strain of Streptococcus pyogenes. The patient, who had undergone a subtotal esophagectomy 4 years previously, was referred to our department after the diagnosis of a metastatic lung tumor. A right lower lobectomy of the lung was performed, and prolonged air leakage from a pulmonary fistula thereafter developed because of the dissection of severe pleural adhesion. OK-432 (5 klinische einheiten) was administered to the pleural cavity 3 times. On the 13th postoperative day, the patient began to complain of general fatigue and nausea. SIADH was diagnosed based on laboratory findings such as hyponatremia, serum hypo-osmolality and a high excretion of sodium in the urine. A restriction of the fluid intake with a sodium supplement resulted in the return to a normal serum level within 2 weeks. We therefore concluded that the intrapleural instillation of OK-432 had apparently caused SIADH in this case, because no other causes could be found.
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PMID:A syndrome of inappropriate secretion of antidiuretic hormone associated with pleuritis caused by OK-432. 973 Aug

Authors deal in detail with the pathophysiology of the osmolal regulation. Besides hyperosmolality the secretion of antidiuretic hormone (ADH) in increased by hypovolemia and hypotension. Secretion of ADH is lowered in hypoosmolal states. All other mechanisms are preferebly volume regulating and they influence mainly retention and excretion of sodium. Authors discuss homeostatic effects of the renin-angiotensin-aldosteron system, effects of renal failure with prevailing glomerular or tubular function disorder, impact of diuretics, natriuretic peptides, digitalis-like hormone, urodilantin and influence of the other solutes. Disorders of the effective osmolality regulation are frequent in the cerebral affections that originate from trauma, vascular disease, inflammation or tumors. Hypoosmolality and hyponatremia are presented in two different conditions: Inappropriate Vasopressin Secretion Syndrome (IADHS) and Cerebral Salt Wasting Syndrome (CSWS). Quick differential diagnose is important because the treatment of both syndromes is essentially different. Typical cause of hypernatremia is central diabetes insipidus (DI). The group of available calculated renal function parameters is applied in the differential diagnosis of these syndromes. They are creatinin clearance, excretion fraction of water and sodium, electrolyte clearance and electrolyte free water clearance. Investigation of ADH and natriuretic peptide could be even misleading. Pathophysiologic consequence of the state given by inappropriate elevation of one hormone can be the elevation of the second one.
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PMID:[Disturbances of effective osmolality regulation in disorders of the central nervous system and possible methods of monitoring]. 974 51

Recent results indicate that renal escape from vasopressin-induced antidiuresis is accompanied by a marked downregulation of whole kidney aquaporin-2 (AQP-2) protein and mRNA expression. However, in those studies, the escaped animals were also markedly hypo-osmolar compared to controls as a result of water loading during antidiuresis. The present studies evaluated whether systemic or local osmolality contributes to the downregulation of AQP-2 expression in this model. In the first study, two groups of 1-deamino-[8-D-arginine]-vasopressin (dDAVP)-infused rats were water-loaded; after establishment of escape, one group was then water-restricted for 4 d to reverse the escape, whereas the other group continued daily water loading. Whole kidney AQP-2 protein was measured by Western blotting, and inner medulla AQP-2 mRNA was determined by Northern blotting. Results were compared to dDAVP-infused rats fed solid chow. After 4 d of water restriction, urine volume decreased to the same level as in the rats on solid chow; however, plasma sodium concentrations and plasma osmolality remained low. Despite maintenance of significant hypo-osmolality, rats in which escape was subsequently reversed by water restriction reestablished high dDAVP-stimulated kidney levels of AQP-2 after 4 d of water restriction. In the second study, AQP-2 expression was evaluated in different regions of kidneys from water-loaded rats undergoing escape from antidiuresis. Despite markedly different interstitial osmolalities, significant downregulation of AQP-2 expression compared to dDAVP-infused control rats was seen in the inner medulla, outer medulla, and cortex. Thus, neither systemic nor interstitial osmolality appears to appreciably be correlated with downregulation of kidney AQP-2 expression during escape from antidiuresis. These results therefore suggest that additional vasopressin- and osmolality-independent factors, likely related to the effects of extracellular fluid volume expansion, also regulate kidney AQP-2 expression in rats.
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PMID:Kidney aquaporin-2 expression during escape from antidiuresis is not related to plasma or tissue osmolality. 1050 82


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