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)

The syndrome of inappropriate secretion of antidiuretic hormone is characterized by production of less than maximally dilute urine in the presence of hypotonic plasma. It may be secondary to malignant disease, central nervous system disorders, or pulmonary disease, among other conditions, or it may be idiopathic. Manifestations are those of water intoxication, eg, confusion, fatigue, nausea, headache, and neurologic signs. The pathogenesis is not completely understood. Restriction of fluid intake to obtain a negative water balance is effective treatment.
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PMID:Inappropriate secretion of antidiuretic hormone. An overview of the syndrome. 90 56

A 44-year-old female with 16-year history of rheumatoid arthritis visited Akiru Hospital with complaints of a thirst, a dry mouth and a general fatigue. One week prior to admission, the patient manifested excessive thirsty feeling, a body weight loss and a sleepless by the polyuria. She has been given 5-10 mg of prednisolone and 240 mg of lobenzarit disodium (CCA) in a day for 11 months. A hematologic examination showed no abnormality, and the examination of her serum showed the following values: BUN, 9.3 mg/dl; creatinine, 0.9 mg/dl; sodium, 139 mEq/l; chloride, 102 mEq/l; potassium, 3.9 mEq/l; osmolality, 290 mOsm/l. Plasma antidiuretic hormone (ADH) level increased slightly (6.0 pg/ml). Examination of her urine revealed specific gravity, 1.005; no trace of glucose, protein, blood and ketones; normal sediment; and osmolality, 209 mOsm/l. The patient was given exogenous ADH (10 units of vasopressin tannate in oil, intramuscularly) to obtain a diagnosis, and she was found to be unable to concentrate her urine more than 1.008 in the specific gravity. A water restriction, as a test for diabetes insipidus, also failed to concentrate her urine in the specific gravity and in the osmolality. Together with these findings, the patient was diagnosed to be a diabetes insipidus, and CCA was seemed to account for the disease. This unfavorable effect of CCA appeared to be reversible, since the patient recovered her urinary concentrating ability after the medication of CCA was discontinued.
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PMID:[Lobenzarit disodium (CCA)--induced diabetes insipidus in a patient with rheumatoid arthritis]. 141 95

Effects of arginine-vasopressin (AVP) and oxytocin (OX) on brainstem and middle latency auditory-evoked potentials (BAEP and MAEP), reflecting early sensory processing within the specific auditory pathways and primary auditory cortex, were investigated. Additionally, subjects rated their feelings of activation and mood on an adjective check list (EWL). The experiments were undertaken in 12 healthy male volunteers, receiving either placebo, 0.15 IU AVP, 0.5 IU AVP or 0.5 IU OX as IV bolus injection according to a within-subject double-blind design. There were no consistent effects of AVP and OX on BAEPs and MAEPs. AVP decreased self-perceived deactivation, fatigue and arousal. Results do not suggest an effect of AVP and OX on early stages of sensory processing, but, consistent with previous studies, demonstrate changes towards increased (self-perceived) general activation following administration of these hormones.
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PMID:Vasopressin and oxytocin do not influence early sensory processing but affect mood and activation in man. 181 25

We report a case of 47-year-old woman with an isolated deficiency of adrenocorticotropic hormone. She was admitted complaining of fatigue and frequent loss of consciousness. The patient developed severe hyponatremia (100 mEq/l) after five days of the admission. Her plasma renin activity and plasma aldosterone concentration were low though she was dehydrated. After the treatment of dehydration, plasma osmolality was low but high plasma antidiuretic hormone (ADH) level sustained. Both high urinary sodium excretion and low urinary aldosterone excretion still remained after one month of replacement therapy with prednisolone. But, glomerular filtration rate and a response of urinary volume to acute water loading were normalized. These results suggested that severe hyponatremia of the patient was caused by an inappropriate secretion of ADH and suppression of renin-aldosterone system. We consider the suppression of renin-aldosterone system was partially independent of an inappropriate secretion of ADH.
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PMID:[Hyponatremia in isolated deficiency of adrenocorticotropic hormone: role of a decrease in aldosterone secretion independent of antidiuretic hormone excess]. 217 15

The renin-angiotensin-aldosterone system plays an important role in the development of congestive heart failure (CHF). In patients with chronic heart failure, angiotensin-converting enzyme (ACE) inhibitors, such as captopril, enalapril, and quinapril, have been shown to improve hemodynamics, reduce symptoms of fatigue and dyspnea, increase exercise capacity, correct hyponatremia, reduce diuretic requirements and ventricular arrhythmias, and conserve potassium and magnesium. ACE inhibitors reduce circulating levels of angiotensin II and aldosterone and may reduce plasma norepinephrine and vasopressin levels. They are equally effective in patients with mild to moderate heart failure and in patients with severe cardiac impairment. ACE inhibitors are at least as beneficial as digitalis in patients with mild heart failure, and they may even be considered as first-line therapy. Promising results have also been obtained in patients with myocardial infarction, in whom long-term therapy with ACE inhibitors has prevented an increase in heart size. ACE inhibitors improve prognosis in patients with severe heart failure and in patients with hyponatremia; the question of effect on survival in mild to moderate heart failure has yet to be answered.
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PMID:ACE inhibitors in congestive heart failure. 267 Feb 20

Capsule-deficient Cryptococcus neoformans (CN-CD) infection is very rare. The authors recently experienced the case of CN-CD infection with the complication of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a 83 year old woman. She was admitted to our hospital with the complaints of fever and general fatigue on June 10, 1987. At the time of admission, there were no abnormal findings except a mildly lowered consciousness level on physical examination, there were no abnormal neurological finding nor meningeal signs. Laboratory data revealed a mild leukocytosis and hyponatremia. Chest X-P showed a few small nodular shadows scattered in both lungs. Antibiotics therapy was of no help and hyponatremia became worse. Then with the suspicion of SIADH, Demeclocycline was administered and limitation of water intake was decreased and hyponatremia improvement was used. Yeast-like fungi was detected in the venous blood culture and in the cerebrospinal fluid (cell count: 252/3) CN-CD by India-ink preparation and bacteriological nature were determined. We made a diagnosis of sepsis and meningitis by CN-CD accompanied with SIADH. In spite of Miconazole administration intravenously and intrathecally, she died 2 months after admission. The minimal inhibitory concentration (micrograms/ml) of antibiotics against the isolated CN-CD was as follows: Amphotericin B: 0.78, 5-PC: 1.56, Miconazole less than or equal to 0.05, Nystatin: 25, Ketoconazole: 0.78.
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PMID:[A case of sepsis and meningitis due to capsule-deficient Cryptococcus neoformans with SIADH]. 269 39

Two cases of miliary tuberculosis with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) were reported. Case 1. A 70-year-old woman suffering from general fatigue and appetite loss developed neck stiffness and stupor three days after admission. The chest X-ray film showed a miliary pattern in both lungs. The lumber puncture showed high pressure and increased leucocytes in the cerebrospinal fluid. Serum natrium concentration was 113 mEq/L. Tubercle bacilli were seen in the broncho-alveolar lavage fluid by the Ziehl-Nielsen staining. An improvement in electrolytes balance was produced by 2.5% NaCl and antituberculous treatment, then her mental function recovered. Case 2. A 71-year-old man was admitted with gastric ulcer. When he developed dry cough thirty days after admission, the chest X-ray film showed a miliary pattern in both lungs. Acute respiratory failure advanced concomitantly. Tubercle bacilli were seen in the sputum (Gaffky 5) by the Ziehl-Nielsen staining. Antituberculous treatment was started. Although the miliary shadow improved gradually, hyponatremia was rather progressing. The following values for serum constituents were determined: sodium, 118 mEq/L; antidiuretic hormone, 10.3 pg/ml. Antituberculous treatment and supplement of NaCl (10 g/day) improved serum natrium level. He had no mental disturbance in his clinical course. In both cases, thyroid, renal and adrenal function were normal. Systemic edema and dehydration did not exist at the state of hyponatremia, and it was very clear that laboratory data were compatible with SIADH criteria. Miliary tuberculosis is one of the least commonly recognized causes of SIADH.
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PMID:[Two cases of miliary tuberculosis with SIADH]. 279 13

Secretion of the peptide neurohormones oxytocin and vasopressin from terminals of magnocellular neurones in the mammalian neurohypophysis is elicited by conduction of depolarizing action potentials into terminal membranes, inducing opening of voltage-sensitive Ca2+ channels, entry of Ca2+ from the extracellular space and a rise in cytoplasmic Ca2+ concentration. The amount of peptide released per action potential is not immutable. In particular, the patterns in which action potentials are generated at the cell somata of the two types of neurone each appear exquisitely suited to optimize the release process at the terminal by utilizing a frequency-facilitation mechanism and by minimizing a mechanism of fatigue in the release process. The different properties of oxytocin and vasopressin neurones are of important physiological significance. The secretory terminals are also a site of receptor-mediated influences of neuromodulators which can greatly alter release efficiency. The mechanisms underlying facilitation and fatigue are not clearly understood. The evidence suggests that processes both prior to depolarization of the terminals (propagation and form of the action potentials) and directly at the terminals (frequency/pattern-dependent Ca2+ entry and channel openings) are involved. Transient activity-related increases in extracellular K+ concentration may be involved at both sites. Two types of neuromodulation have been partly characterized. Kappa-Opioid receptors in secretory terminal membranes directly modulate depolarization-evoked peptide release probably via interactions with Ca2+ channels. beta-Adrenergic receptors localized on neurohypophyseal astroglial cells mediate more subtle effects of noradrenaline. In the more chronic situation the neurohypophyseal astroglia alter their morphological relationships with neurosecretory elements and the basal lamina at release sites, changes which may also serve to optimize the secretory process.
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PMID:Optimizing release from peptide hormone secretory nerve terminals. 285 Mar 39

A case of hyponatremia is presented with water intoxication due to treatment with oxcarbazepine (OxCZ). The patient was admitted because of exceeding dullness and increasing seizures. Low values for serum sodium and osmolality were found. Simultaneously with the reduction in OxCZ, values of sodium and osmolality increased, normalizing on discontinuation of the drug, and the exceeding tiredness as well as the generalized seizures disappeared. Low values of arginine-vasopressin were found, suggesting that the mode of action of OxCZ was directly or indirectly at the level of the kidney.
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PMID:Hyponatremia induced by oxcarbazepine. 314 48

1. Isolated rat neurohypophyses were fixed by their stalks to a platinum wire electrode and superfused with oxygenated Krebs-HEPES solution. Vasopressin release into the medium was determined by radioimmunoassay. Vasopressin secretion was increased by electrical stimulation at different frequencies (3-30 Hz) and different train lengths (75-900 pulses). The effects of tetraethylammonium (TEA) ions and of enhanced calcium were tested. 2. Electrical stimulation at 7.5 or 15 Hz evoked a markedly larger release of vasopressin than stimulation at 3 Hz. During continuous stimulation at 7.5 and 15 Hz the evoked vasopressin release per pulse declined rapidly, but with similar time constants for both frequencies indicating that the fatigue of the release process was strongly time dependent. The kinetic analysis showed also that the initial release per pulse was identical for 7.5 and 15 Hz stimulation. Nevertheless, with increasing duration, stimulation at 7.5 Hz became less efficient (in terms of release per total stimulus) than stimulation at 15 Hz and this was due to the time-dependent fatigue. 3. TEA (10 mM) increased the release of vasopressin evoked by 3 Hz stimulation much more than that evoked by 15 Hz stimulation resulting in an equieffective activation of release by both stimuli. On the other hand, elevation of the extracellular calcium from 1.2 to 3 mM did not alter the different efficiency of stimuli of 3 and 15 Hz. In the presence of TEA the time-dependent fatigue of the release during continuous stimulation was prevented, but an additional, slower component of the fatigue became apparent which was release or impulse dependent. 4. As prolongation of the action potential by TEA facilitates preferentially the hormone release evoked by low (ineffective) frequencies, it is suggested that a frequency-dependent broadening of action potentials which reportedly occurs on neurosecretory neurones may play an important role in the frequency-dependent facilitation of hormone release from the rat neurohypophysis.
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PMID:Effects of tetraethylammonium ions on frequency-dependent vasopressin release from the rat neurohypophysis. 341 19


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