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)

Nine episodes of the syndrome of inappropriate antidiuretic hormone secretion occurred in five newborn infants following atelectasis or pneumothorax. All infants had pre-existing lung disease and were being treated with positive pressure ventilation. The mean interval between acute atelectasis or pneumothorax and the development of diagnostic hyponatremia, hypo-osmolal serum, hyperosmolal urine, and oliguria was 13.4 hours. Fluid restriction and removal of the triggering event resulted in resolution of the abnormalities within 1.5 to 4 days. Infants who develop atelectasis or pneumothorax should be evaluated for the subsequent occurrence of SIADH; the administration of a water load to them may result in dilutional hyponatremia, for which fluid restriction, not sodium infusion, is the proper therapy.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion in neonates with pneumothorax or atelectasis. 89 20

The role of antidiuretic hormone (ADH) in the pathogenesis of renal impaired water excretion in acute respiratory failure has not been clearly delineated. Plasma sodium concentration and plasma ADH levels (radioimmunoassay) were therefore serially measured in 13 patients with acute respiratory failure (10 with acute exacerbations of chronic lung disease and three with acute lung disease) and eight "control" patients admitted ot the intensive care unit with suspected myocardial infarction. None of the patients had systemic hemodynamic, hepatic or renal dysfunction. ADH levels were significantly elevated in patients with acute respiratory failure (15.1 +/- 5.2 pg/ml versus 5.7 +/- 1.9 pg/ml, p less than 0.05) when compared with levels in control patients. The elevated ADH levels occurred despite significantly lower plasma sodium concentration (133 +/- 1 meq/liter versus 138 +/- 2 meq/liter, p less than 0.05) compared wit control values. Moreover, markedly increased ADH values (range 1.1 to 13.0 pg/ml) were often encountered in patients with acute respiratory failure despite significant hyposmolality (263 to 275 mOsm/kg H2O). This was not observed in any control patients. These results suggest that patients with acute respiratory failure are susceptible to water retention and hyposmolality due to nonosmotic release of antidiuretic hormone.
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PMID:Plasma antidiuretic hormone in acute respiratory failure. 707 43

We report a 59-year-old man with cryptococcal meningoencephalitis who presented with typical features of syndrome of inappropriate antidiuretic hormone secretion (SIADH). There was no evidence of lung disease or drugs causing SIADH. Studies for endocrine functions and tumor markers were normal. The patient's hyponatremia was refractory to treatment (Na 120-125 mmol/L) after resolution of the cryptococcal infection. Three months after completion of antifungal treatment, a radiograph of the chest disclosed widening of the mediastinum. Computed tomography revealed a mediastinal mass. A tentative diagnosis of extrapulmonary cryptococcoma or a tumor was made. Positron emission tomography using F-fluorodeoxy glucose demonstrated an intense uptake mass in the mediastinum without lesions elsewhere in the body. A biopsy of the mass clearly showed small cell carcinoma (SCC) with positive immunoreactivity for arginine vasopressin and atrial natriuretic peptide. The hyponatremia completely resolved and tumor size dramatically decreased after chemotherapy. To the best of our knowledge, this is the first case of mediastinal SCC associated with SIADH. Patients with otherwise unexplained SIADH should be meticulously scrutinized for a possible malignancy.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion in a patient with cryptococcal meningoencephalitis: a hidden mediastinal small cell carcinoma. 1670 2

In recent years, transgenic mouse models have been developed to examine the underlying cellular and molecular mechanisms of lung disease and pulmonary vascular disease, such as asthma, pulmonary thromboembolic disease, and pulmonary hypertension. However, there has not been systematic characterization of the basic physiological pulmonary vascular reactivity in normal and transgenic mice. This represents an intellectual "gap", since it is important to characterize basic murine pulmonary vascular reactivity in response to various contractile and relaxant factors to which the pulmonary vasculature is exposed under physiological conditions. The present study evaluates excitation- and pharmacomechanical-contraction coupling in pulmonary arteries (PA) isolated from wild-type BALB/c mice. We demonstrate that both pharmaco- and electromechanical coupling mechanisms exist in mice PA. These arteries are also reactive to stimulation by alpha(1)-adrenergic agonists, serotonin, endothelin-1, vasopressin, and U-46619 (a thromboxane A(2) analog). We conclude that the basic vascular responsiveness of mouse PA is similar to those observed in PA of other species, including rat, pig, and human, albeit on a different scale and to varying amplitudes.
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PMID:Characterization of agonist-induced vasoconstriction in mouse pulmonary artery. 1798 12