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 antidiuretic hormone secretion (SIADH) developed approximately 7 days after a spontaneous subarachnoid hemorrhage in a 63-year-old woman with an anterior cerebral artery aneurysm. The hyponatremia associated with this syndrome resulted in a deterioration of the patient's clinical condition and focal neurological signs, which simulated the clinical deterioration after spontaneous subarachnoid hemorrhage that is often caused by other intracranial pathological conditions. The focal neurological signs in particular are likely to be interpreted as indicating one of these other conditions. Prompt recognition and treatment of the SIADH resulted in prompt improvement, and we were then able to proceed with the planned craniotomy for the aneurysm. The syndrome and its importance are discussed.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion after spontaneous subarachnoid hemorrhage: a reversible cause of clinical deterioration. 74 Jan 40

In addition to progressive endocrine dysfunction and progressive visual loss, pituitary neoplasms may annouce their presence by the more catastrophic alternative of spontaneous tumor infarction. In two patients reported, illness due to the spontaneous infraction of pituitary tumors was heralded by sudden onset of focal headache associated with diplopia. Stupor, confusion, and evidence of increased intracranial pressure occurred without subarachnoid hemorrhage or massive extrasellar extension of tumor. One patient developed inappropriate antidiuretic hormone secretion with spontaneous infarction in a large but clinically silent chromophobe adenoma. In both patients, skull x-rays suggested a long-standing intrasella mass. Both underwent prompt treatment with endocrinologic replacement therapy and subsequent successful transsphenoidal removal of voluminous, infarcted, pituitary masses.
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PMID:Spontaneous infarction in pituitary tumors: neurologic and therapeutic aspects. 116 78

The cause of hyponatremia following subarachnoid hemorrhage (SAH) has been understood as an inappropriate secretion of antidiuretic hormone (SIADH). Whereas, water restriction for the management of this condition sometimes induces a severe dehydration, resulting in vasospasm. To clarify the pathogenesis of hyponatremia following SAH, we measured the daily sodium and water balance with the plasma concentration of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in seventeen cases after subarachnoid hemorrhage. Although the patients received an adequate amount of fluid (more than 4080ml/day; daily average in seventeen cases) and sodium (more than 277 mEq/day; daily average in seventeen cases), eight out of the seventeen cases showed transient hyponatremia of a slight degree beginning on 8.8 days after SAH. ANP values were elevated markedly in fifteen out of the seventeen cases, remaining high during the first two weeks following SAH. ADH values were elevated remarkably in eight out of the seventeen cases. However, these values declined immediately to a normal range within two days following SAH. PRA were increased or came within the normal range, suggesting the lack of water retention. Overall sodium balance and water balance did not differ significantly between hyponatremia cases and normonatremia ones, whereas, sodium balance in acute phase was significantly negative, associated with marked natriuresis in patients with hyponatremia. These correlations suggested that hyponatremia after SAH is the result of natriuresis by an increased ANP rather than ADH. In conclusion, a greater replenishment of water and sodium is required to avoid hyponatremia with dehydration. This technique may be helpful for the prevention of vasospasms following SAH.
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PMID:[Pathogenesis of hyponatremia observed in the treatment of acute subarachnoid hemorrhage]. 128 91

Endothelins (ET-1, ET-2 and ET-3) are a family of 21 amino acid peptides produced by endothelial cells. They are thought to regulate the local vasomotor tone with endothelium-derived relaxing factors. ETs are the most potent vasoconstrictor substances yet identified and veins and renal vasculature are the most sensitive targets. They reduce cardiac output and have positive inotropic and chronotropic effects. ETs increase the secretion of atrial natriuretic peptide (ANP), aldosterone and catecholamines but reduce renal blood flow and glomerular filtration and they also have mitogenic properties. ETs bind to receptors (ETA and ETB), activate phospholipase C, modulate intracellular Ca2+ concentration and open Ca2+ channels. Vasoactive agents (adrenaline, angiotensin, vasopressin, thrombin, endotoxins) and hypoxia stimulate the release of ET and also ET gene expression. Raised concentrations of plasma ET have been found to occur in several clinical conditions such as hypertension, myocardial infarction, cardiogenic shock, pregnancy induced hypertension, arteriosclerosis, Raynaud's disease, subarachnoid haemorrhage, uraemia, ulcerative colitis, Crohn's disease and surgical operations suggesting that ETs have a role in several patophysiological processes.
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PMID:Endothelin peptides: biological activities, cellular signalling and clinical significance. 138 14

We have examined the total number of admitted cases to clarify the pathogenesis of hyponatremia during the management of neurosurgical patients. We experienced 32 cases of hyponatremia during the past year by measuring the sodium balance and atrial natriuretic peptide (ANP) level. According to these two factors, we divided the cases into three groups. The first group shows normal ANP levels in spite of hyponatremia. Low administration of the sodium was thought to be the cause in these cases. The second group shows the elevated ANP levels with a positive sodium balance. Elevated circulatory volume due to the inadequate level of antidiuretic hormone and mild heart and/or kidney failures cause these conditions. Water restriction and/or diuresis were effective methods in the management of the cases. The last group shows the elevated ANP levels with a negative sodium balance. There is a statistically significant negative correlation between sodium balance and the ANP level. Marked natriuresis due to the elevated ANP causes the decrement of the circulatory volume in these cases. Pathogenesis of the last group is very important in the management of neurosurgical patients in an acute state, especially in subarachnoid hemorrhage cases. The decrement of the systemic circulatory volume would jeopardize the patient's neurological condition. In this group, water restriction that has been commonly recommended is contraindicated. Satisfactory water and sodium replenishment seems to be the best recommended treatment for this group.
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PMID:[Significance of plasma atrial natriuretic peptide measurement during the management of hyponatremia in neurosurgical patients]. 138 69

The CNS plays an integral role in the neuroendocrine regulation of sodium and water homeostasis. Therefore, disturbances of this function are common in patients with CNS disease. The body's sodium and water content are tightly regulated in order to maintain normal osmolality and intravascular volume. Complex neural, humoral, and renal mechanisms integrate information regarding osmolality, intravascular volume, blood pressure, and intake of sodium and water. They act to modify intake and excretion of sodium and water and vascular tone. Most sodium abnormalities in patients with CNS disease result from altered water excretion secondary to disturbed release of antidiuretic hormone (ADH). Insufficient release is seen with lesions in or near the optic chiasm and pituitary gland and results in diabetes insipidus (DI). DI is common following surgery or trauma in this region and care must be exercised in treating these patients because of the potentially variable and transient nature of the disturbance. The syndrome of inappropriate release of ADH is seen in a wide variety of CNS disorders and produces a dilutional hyponatremia. Symptomatic hyponatremia should be managed aggressively with diuretics and hypertonic saline followed by fluid restriction. However, very rapid correction or overcorrection should be avoided. In some patients, especially those with acute subarachnoid hemorrhage, disturbed sodium regulation appears to contribute to hyponatremia. Patients with subarachnoid hemorrhage and hyponatremia should not be fluid restricted, because of the risk of exacerbating vasospasm, but treated with large volumes of isotonic saline.
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PMID:Management of sodium abnormalities in patients with CNS disease. 147 46

In vivo experiments on the vasoactive effects of vasopressin and oxytocin on cerebral circulation were carried out in anesthetized dogs, using an electromagnetic flowmeter to measure vertebral blood flow and angiography to measure the internal diameter of the basilar artery. Direct bolus infusion of 1 pmol to 1 nmol of vasopressin or 10 pmol to 10 nmol of oxytocin into a femoral-vertebral artery shunt produced a dose-dependent decrease in vertebral artery blood flow without significantly affecting mean arterial blood pressure. Vasopressin was more potent than endothelin and neuropeptide Y, which have also been demonstrated to induce long-lasting decreases in vertebral artery blood flow. However, direct bolus infusion of vasopressin (100 pmol and 1 nmol) or oxytocin (1 nmol and 10 nmol) into the vertebral artery dilated major vessels including the vertebral, anterior spinal, and basilar arteries, as well as the circle of Willis and its main branches, while endothelin (1 nmol) and neuropeptide Y (5 nmol) caused no change in the diameters of major cerebral arteries. The V1 antagonist d(CH2)5tyrosine(methyl) arginine vasopressin suppressed the effects of both vasopressin and oxytocin. Vasopressin was over 10 times as potent as oxytocin in both assays. The vasodilatory effect of vasopressin, which may be mediated by an endothelium-dependent mechanism, was functionally damaged in dogs after experimental subarachnoid hemorrhage. These data suggest regional differences in the sensitivity and responsiveness of vasculature to vasopressin and oxytocin, and specifically that both peptides act through V1 receptors to decrease the resistance of large vessels and increase the resistance of small vessels.
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PMID:Effects of vasopressin and oxytocin on canine cerebral circulation in vivo. 150 90

For intracranial diseases, plasma atrial natriuretic peptide (ANP), antidiuretic hormone (ADH) and aldosterone were determined and their effects on the development of hyponatremia with central origin were studied. The subjects were 71 cases of intracranial diseases which were admitted to our hospital during a period of 1 year from March, 1989 to March, 1990. The diseases were broken down to subarachnoid hemorrhage 26 cases, hypertensive intracerebral hemorrhage 19 cases, head injury 12 cases, cerebral infarction 11 cases and 3 other cases. Serum-urine electrolytes, plasma ANP and ADH were determined in the acute stage on Day 1 to 4, in the hyponatremia stage on Day 5 to 14 and in the chronic stage on Day 15 downward. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less. Cases evidently having other causes such as heart failure and renal insufficiency were excluded. In the normal control group of persons who were admitted to our hospital for a close checkup (n = 20), plasma ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of 50 pg/ml or more were regarded as abnormally high. 1) Hyponatremia was found in 18 cases (25.4%), subarachnoid hemorrhage in 7 cases, hypertensive intracerebral hemorrhage in 4 cases, head injury in 5 cases and others in 2 cases. 2) The time of onset of hyponatremia was on the 8.3 hospital day. The duration was 7.2 days. The minimum serum sodium level was 124.6 mEq/l. 3) There was no significant change in the plasma aldosterone level at each stage.2+ Predicting development of hyponatremia from plasma ADH and ANP levels in the acute stage is difficult. Inadequate secretion of ANP rather than ADH appeared to be an important factor for the development of hyponatremia, but the plasma ANP level was not always abnormally high, so involvement of other sodium diuretic factors should also be kept in mind.
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PMID:[A study of plasma atrial natriuretic peptide, antidiuretic hormone and aldosterone levels in a series of patients with intracranial disease and hyponatremia]. 153 80

Hyponatremia is common following subarachnoid hemorrhage and has alternatively been attributed to either the inappropriate secretion of antidiuretic hormone or natriuresis causing intravascular volume contraction. We prospectively studied body sodium and intravascular volume regulation in 19 patients, beginning within 3 days after acute aneurysmal subarachnoid hemorrhage occurred, in order to determine the impact of hypervolemic therapy on both hyponatremia and volume contraction and to ascertain whether humoral factors account for hyponatremia. Serial measurements of plasma arginine vasopressin, atrial natriuretic factor, renin activity, aldosterone, and catecholamines were correlated with body sodium and fluid balance, change in blood volume, serum sodium concentration, and osmolality. Six patients (32%) developed hyponatremia, but only 2 had a negative sodium balance. In most patients, levels of atrial natriuretic factor were elevated, while plasma renin activity and aldosterone concentrations were generally suppressed. Plasma arginine vasopressin levels were not suppressed during hypo-osmolality and did not correlate with serum osmolality in hyponatremic patients. Only 1 patient had a decrease in blood volume, which was associated with marked rises in aldosterone and plasma renin activity, but normal serum sodium and plasma atrial natriuretic factor levels. We conclude that following subarachnoid hemorrhage: (1) Hypervolemic therapy prevents volume contraction but not hyponatremia, (2) humoral factors may favor both sodium loss and water retention, and (3) arginine vasopressin regulation is disturbed and may contribute to hyponatremia.
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PMID:Hypervolemic therapy prevents volume contraction but not hyponatremia following subarachnoid hemorrhage. 153 78

Vascular endothelial cells of the basilar artery and secretory axons of the neurohypophysis from rabbits after experimental subarachnoid haemorrhage were investigated by postembedding peroxidase--anti-peroxidase technique for electron microscopy to detection of vasopressin (VP). The results indicate an lack of VP-positive endothelial cells in basilar artery, while VP-positive secretory granules were commonly present in the neurohypophysis. The results are discussed in terms of pathophysiological aspect of subarachnoid haemorrhage.
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PMID:An electron immunocytochemical study of the basilar artery in rabbits after subarachnoid haemorrhage (SAH): a preliminary report. 225 62


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