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)

A relationship between acute psychosis, water ingestion, and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) has been reported. This syndrome was observed in a psychotic patient who ingested massive amounts of water and became symptomatically hyponatremic with seizures. Although he had been taking haloperidol, the SIADH responded to fluid restriction alone. SIADH was clearly established, and a temporal relationship to his acute exacerbation of psychosis and polydipsia could be shown. This case illustrates that psychosis, polydipsia, and SIADH are often associated as a triad, and that psychiatric history must be considered in the evaluation of this syndrome.
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PMID:Acute psychosis, polydipsia, and inappropriate secretion of antidiuretic hormone. 662 81

A 54-year-old woman had seizures and a focal neurologic deficit associated with hyponatremia induced by a thiazide diuretic. Prompt correction of hyponatremia by administration of hypertonic saline solution was followed by resolution of all neurologic defects. Metabolic balance studies and rechallenge with hydrochlorothiazide were undertaken to investigate the mechanism of the thiazide-induced hyponatremia. Abnormal vasopressin secretion was shown by a plasma vasopressin concentration of 0.5 microU/ml with a plasma osmolality of 268 mOsm/kg water after administration of a fluid challenge consisting of 45 ml/kg body weight. Rechallenge with chlorothiazide while on a sodium- and potassium-controlled balanced diet resulted in a decrease in serum sodium concentration (136 to 124 mEq/L) and plasma osmolality (283 to 261 mOsm/kg) within 18 hours. During this period, urine losses of monovalent cation were only 55 mEq and body weight was constant at 48.2 kg. A second challenge while the patient received all fluids and electrolytes intravenously again resulted in decreased serum sodium concentration (134 to 126 mEq/L) after urinary loss of only 69 mEq of cation. Thus this patient's hyponatremia cannot be accounted for solely by changes in external water and electrolyte balance; the rapidity with which changes were produced suggests that osmolar inactivation, probably intracellularly, may contribute to the severe hypotonicity seen in some patients.
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PMID:Thiazide-induced hyponatremia. 663 23

When pyrogenic substances are injected intravenously into experimental animals, a sequence of events is set in motion which involves the hypothalamus and perhaps other portions of the diencephalon to produce a febrile response. We now present evidence that the brain produces its own endogenous antipyretic which may serve as a means of controlling the extent of the fever. When arginine vasopressin is perfused through the lateral septal area of the hypothalamus of the sheep, fever is suppressed. Vasopressin alone does not lower normal body temperature when perfused through this region of the brain. In addition, evidence is provided to indicate that vasopressin is released within the lateral septal area during the febrile response. It is concluded that, in fever, arginine vasopressin may be released in the lateral septal area of the brain and serve as an endogenous antipyretic. Results indicate that, following an initial application of vasopressin into the brain itself, a subsequent similar administration of vasopressin produces seizure-like activity. Therefore, it is suggested that this release of arginine vasopressin may contribute to the production of febrile convulsion.
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PMID:Vasopressin: its role in antipyresis and febrile convulsion. 672 95

The neurologic changes following lightning injury include coma with cerebral edema, inappropriate secretion of antidiuretic hormone (ADH), seizures, cerebellar ataxia, and painful sensory disturbances. Deteriorating neurologic status may warrant the use of intracranial pressure monitoring devices. Myocardial injury and transient hypertension are generally evident at the onset. Monitoring of the cardiac rhythm may be needed for as long as a week for late onset arrythmia. Abnormalities of memory, mood, and affect noted on recovery of consciousness may persist for months, necessitating close psychiatric and neurlologic follow-up.
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PMID:Neurologic, psychiatric, and cardiovascular complications in children struck by lightning. 692 48

A 6-year-old girl developed generalized seizures followed by coma, five days after surgical removal of a craniopharyngioma. Low serum sodium levels and low serum osmolality with inappropriately high urinary sodium output confirmed the diagnosis of inappropriate antidiuretic hormone (ADH) secretion. Treatment with 3% hypertonic saline solution and repeated doses of furosemide (1 mg/kg) improved her clinical condition; serum sodium levels, however, rose slowly and urinary excretion remained high. Deoxycorticosterone acetate (DOCA), 4 mg/sq m/day, was added to the above regimen. A striking clinical improvement was noted. Serum sodium levels returned to normal with a concomitant sharp decline in urinary sodium output. The clinical course of this patient demonstrates the efficacy of the addition of deoxycorticosterone acetate to hypertonic saline and furosemide in the treatment of severe, life-threatening hyponatremia due to the syndrome of inappropriate antidiuretic hormone secretion.
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PMID:Combined treatment of severe hyponatremia due to inappropriate antidiuretic hormone secretion. 707 19

The cardiovascular effects of opioid peptides have been studied. Leucine-enkephalin (Leu-ENK) produced blood pressure (BP) increases following administration into the lateral brain ventricles (i.v.t.), into the cisterna magna (i.c.i.), and following intravenous (i.v.) administration. Heart rate (HR) increases were observed following all routes of administration (threshold for BP and HR effects at 0.3 nmole, maximum at 360 nmoles). The cardiovascular effects were independent of generalized seizures, which may occur at higher doses of enkephalins (ENK). D-alanine-enkephalin (D-Ala-ENK) attenuated the vagal component of the baroreceptor reflex in cats. This was indicated by the findings that HR did not decrease following D-Ala-ENK-induced BP increases and that the compensatory decreases in HR following i.v. pressor doses of angiotensin II (ANG II) were markedly attenuated in cats treated with i.v.t. D-Ala-ENK. Naloxone inhibited the BP and HR effects following i.c.i. and i.v., but not following i.v.t., administration of Leu-ENK. The i.v.t. Leu-ENK effect were inhibited by beta-adrenergic receptor blockade. Bratteboro rats homozygous for hereditary diabetes insipidus with total absence of antidiuretic hormone (ADH) synthesis responded with BP decreases following i.v.t. Leu-ENK, while BP increases were observed in control Long-Evans rats. Blood pressure increases to i.v.t. Leu-ENK were markedly greater in spontaneously hypertensive rats of the stroke-prone strain (SHR-sp) than in normotensive control rats; SHR-sp exhibit a humoral pattern of increased ADH, ACTH, and catecholamines, presumably due to central peptidergic stimulation. The known effects of opioid peptides on these hormones and the observed cardiovascular responses suggest a possible participation of this peptide system in the maintenance of high BP in the SHR-sp.
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PMID:Enkephalin effects on blood pressure, heart rate, and baroreceptor reflex. 739 23

When vasopressin is administered into the lateral ventricles of rats it produces severe convulsive activity characterized by a rapid barrel rotation. Electrical recordings from the dorsal hippocampus indicate marked elevations in the amplitude and frequency at doses of 5 microliter of 2 x 10(-5) M vasopressin. No significant behavioral effects were noted with oxytocin, somatostatin, beta-melanophore-stimulating hormone, adrenocorticotropin, or leu-enkephalin. Pretreatment of the rats with intraventricularly administered oxytocin, beta-MSH, or systemically administered Dilantin prevented the vasopressin-induced seizures. With the use of chemical and enzymic modification procedures, the essential fragment and amino acids of vasopressin needed for the activity were determined. It was concluded that although the peptide could be acting by vasoconstricting blood arterioles and capillaries in the brain, it may also be exerting a direct excitatory action on neurons.
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PMID:Chemical requirements of vasopressins for barrel rotation convulsions and reversal by oxytocin. 740 Nov 98

Twenty psychotic patients with psychogenic polydipsia had hyponatremia (98 to 124 mEq/L) lasting up to 28 months, with headache, hypertension, dementia, seizures, lethargy, and coma. Two deaths also may be attributed to this syndrome. Patients drank 7 to 43 L of water daily. Urine was dilute during this water load (37 to 95 mOsm/kg), and free water clearance ranged from 12 to 36 L/day, while plasma osmolality was 236 to 244 mOsm/kg. During fluid deprivation in seven such patients, urinary osmolality exceeded plasma osmolality when plasma concentration had risen to between 242 and 272 mOsm/kg, thus suggesting a "reset osmostat" or antidiuretic hormone response to nonosmotic stimuli. This tended to sustain hyponatremia. Polydipsia should be recognized as a cause of hyponatremia, perhaps with reset osmostat. This ultimately may cause dementia or death, possibly secondary to recurrent cerebral edema. This sequence of events is potentially preventable or correctable.
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PMID:Hyponatremia in psychogenic polydipsia. 745 96

The physiology of the release of antidiuretic hormone (ADH) from the posterior pituitary is briefly reviewed. The importance of both osmolar and non-osmolar stimuli is emphasised. Osmolar and non-osmolar factors usually reinforce each other; for example, hydropenia leads to hyperosmolality and hypovolaemia, both promoting ADH release, while hydration has the opposite effect. In disease, osmolar and non-osmolar factors may become dissociated leading to baroreceptor-mediated ADH release in the presence of hyponatraemia and hypo-osmolality. Examples include heart failure, glucocorticoid or thyroxine deficiency, hepatic cirrhosis and nephrotic syndrome with or without the superimposed effect of diuretics, i.e. conditions in which circulatory, and in particular effective arterial, volume is reduced. It is dangerous to label such conditions as 'inappropriate' secretion of ADH since the maintenance of circulating volume is at least as important a physiological requirement as the defence of tonicity. The syndrome of inappropriate secretion of ADH (SIADH) is uncommon in childhood and should only be diagnosed when physiological release of ADH in response to non-osmolar as well as osmolar factors has been excluded. Criteria for the correct identification of SIADH are discussed; the presence of continuing urinary sodium excretion in the presence of hyponatraemia and hypo-osmolality is essential to the diagnosis. SIADH in children is usually due to intracranial disease or injury. The mainstay of treatment is water restriction which reverses all the physiological abnormalities of the condition. Hypertonic saline is rarely indicated for the short-term control of neurological manifestations such as seizures. Drugs have little or no place in the treatment of SIADH in children.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone. 861 39

A 32-year-old woman was bedridden for a year because of chronic pain and headaches. She had insomnia, depression, suicidal thoughts and a severe chemical allergy. She had been on steroid therapy for two years and became Cushingoid with striae in the arm pits, groins and abdomen. However, she had no hypertension, nor the buffalo fat and hirsutism. She was very edematous, with a weight gain from 112 to 180 lbs. The fluid retention did not conform to the syndrome of inappropriate antidiuretic hormone. Studies revealed abnormal scalp EEG discharges and high-voltage seizure discharges in the posterior thalamus. Electrothalamic stimulation suppressed the thalamic discharges and relieved the patient's pelvic pain and headaches. After one month of several thalamic stimulations per day, she was able to get out of bed and ambulate. In addition, the patient no longer was edematous and was tolerating perfumes and floor detergents. Steroids were progressively reduced without complications of withdrawal. She went from a completely steroid dependent state to independent during the first 1-1/2 yrs of thalamic stimulation. With continued thalamic stimulation she has done well for 8-1/2 yrs, weighs 112 lbs, keeps house and drives a car. It's speculated the illness is a chronic pain multiple syndrome predominantly due to mesothalamic discharges and body infirmities. The mesothalamic discharge implicated neural networks, which represent biologic systems, i.e. pain, sleep, fluid retention, etc. Therapeutic stimulation attenuates the discharges and the neural networks return to their normal set points of homeostasis.
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PMID:Mesothalamic discharge in a chronic pain, allergy and fluid retention syndrome (case report). 766 2


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