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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred fourteen patients with ruptured cerebral aneurysms were reviewed in regard to the incidence and etiological factors of preoperative disturbances of water and electrolyte metabolism. Patients with inadequate salt intake, evidence of renal disease, cardiac failure or excessive diuretic therapy were excluded. Twenty-five (21.9%) patients developed water and electrolyte disturbances. Hyponatremia (less than 130 mEq/l) occurred in 18 (15.8%) of 114 patients. The majority of those patients with hyponatremia showed laboratory findings and/or clinical features suggesting the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The mean interval between the last subarachnoid hemorrhage (SAH) and the development of hyponatremia was 13.5 days (range 6 to 26 days). No patients developed hypernatremia (more than 155 mEq/l). Preoperative diabetes insipidus (DI) occurred in 7 (6.1%) of 114 patients. The mean interval between the last SAH and the onset of DI was 26.5 days (range 15 to 35 days). When compared with the onset of hyponatremia following SAH, the development of DI was significantly delayed. The present study showed that the following five types of patients significantly related to the development of preoperative water and electrolyte disturbances after SAH due to cerebral aneurysms. The patients with ruptured aneurysms of anterior communicating, anterior cerebral artery or internal carotid artery. The patients in grade III, IV according to Hunt & Hess. The patients with high density in the basal subarachnoid space on the CT scan. The patients with a small hematoma in the region of the basal frontal interhemispheric fissure in cases with aneurysms of the anterior communicating or anterior cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Etiology of water and electrolyte metabolism imbalance following the rupture of cerebral aneurysms--with special reference to preoperative condition]. 646 63

The use of vasopressin to limit the polyuria of the brain-dead organ donor is a controversial subject. It is held that the associated vasoconstriction may result in ischemic damage to transplantable organs. However, the derangements in the intravascular--and thereby interstitial and intracellular--fluid and electrolyte balances associated with diabetes insipidus may lead to gross fluid shifts in the organ donor. Aggressive resuscitation with crystalloid solutions may aggravate these fluid shifts, contribute to the development of interstitial and intracellular edema, and ultimately result in cardiovascular failure and the rejection of the organs for transplantation. Theoretically, a minute amount of vasopressin is required for the maintenance of normal intravascular fluid and electrolyte balance, and it is best administered as a continuous i.v. infusion. We report on our study of an animal model of a brain-dead organ donor, in which polyuria, hypernatremia, and hyperosmolality developed. The administration of low-dose (2-10 microU/kg/min) vasopressin by continuous infusion maintained plasma sodium and osmolality in the normal range over the course of the experiments (24 hr) in the experimental group. Cardiovascular function remained stable in both control and experimental vasopressin-infusion) groups, with the only significant difference being a moderate rise in pulmonary artery pressure. It would appear that early low-dose vasopressin supplementation by continuous i.v. infusion may improve donor management. The maintenance of intravascular homeostasis may contribute to the quality and number of organs for transplantation.
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PMID:Vasopressin supplementation in a porcine model of brain-dead potential organ donors. 649 67

Within the anterior wall of the third cerebral ventricle, structures are found which have been implicated in the regulation of fluid and electrolyte balance. These structures include the subfornical organ (SFO), preoptic medianus nucleus (PMN) and the organum vasculosum of the lamina terminalis (OVLT). In sheep, the OVLT rises from the ventricular floor over the optic chiasma and occupies most of the midline ventricular wall up to the level of anterior commissure. It contains a plexus of blood vessels at its base which possess fenestrated endothelial cells, and appears to lack ependyma. The SFO of sheep bulges into the third ventricle above the anterior commissure and the PMN is situated between the SFO and OVLT, surrounding the rostral edge of the midline anterior commissure. Like most mammals, water deprivation in sheep results in hypertonicity of body fluids, thirst and graded increase in plasma concentration of vasopressin (AVP). Dehydration also causes a natriuresis in these animals. In sheep with combined ablation of OVLT/PMN tissue, the volume of water drunk, the increases in plasma vasopressin (AVP) level, and the natriuresis in response to dehydration were considerably attenuated, and extreme hypernatremia resulted. Additionally, ablation of OVLT/PMN tissue almost abolished water drinking and AVP secretion in response to systemic infusion of hypertonic NaCl, but did not diminish AVP secretion in response to haemorrhage. In other animals, the OVLT and PMN were individually ablated. While partial osmoregulatory deficits were observed in each case, these deficits were smaller than those observed with combined OVLT/PMN ablation. In contrast to these results, the homeostatic responses to dehydration were not diminished in sheep with combined SFO/PMN lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The anterior wall of the third cerebral ventricle and homeostatic responses to dehydration. 653 50

The role of arginine-vasopressin (AVP) in the pathogenesis of deoxycorticosterone acetate (DOCA) salt hypertension in rats was studied with AVP receptor antagonists for its tubular (V2) and/or vascular (V1) actions. When chronic (six weeks) infusion of the antagonists was started concomitantly with DOCA-salt treatment the development of hypertension was attenuated by the V1-antagonist and prevented by the V1V2-antagonist. However, the V1V2-antagonist induced severe and persistent hypernatraemia in all rats. When chronic (two weeks) infusion of the antagonists was started in rats with established hypertension after five weeks of DOCA-salt treatment blood pressure was not influenced by the V1-antagonist. The rats which received the V1V2-antagonist died from hypernatraemia within four days. These results suggest that in DOCA-salt treated rats AVP is essential for the prevention of severe and life-threatening hypernatraemia. AVP appears to contribute significantly to the development of this form of hypertension through both its vascular and tubular effects.
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PMID:Contribution of vascular and tubular effects of arginine-vasopressin to the development of deoxycorticosterone acetate (DOCA)-salt hypertension in rats. 659 76

Here we have reviewed mainly the cerebral regulation of water intake and its relationship with the regulation of the water-retaining antidiuretic hormone (ADH). Much new information of obvious interest has been gained by experiments in conscious animals, by studies in healthy humans, and by clinical investigations. Of particularly great value has been the development of a sensitive radioimmunoassay for determination of plasma ADH (59). The sketchy picture that emerges in light of this new information is as follows. The osmotic regulation of water intake and ADH secretion is exerted by juxtacerebroventricular sensors apparently mainly located on the anterior border of the third ventricle. These sensors may be accessible both to CSF-borne and blood-borne stimuli and inhibitors, and their activity seems to be correlated to the Na concentration of the ECF rather than to its tonicity. A less sensitive volume regulation of water intake and ADH secretion is effectuated by cardiovascular distention and pressure receptors monitoring the effective circulating blood volume, and in severe volume depletion states also by the renin-angiotensin system (RAS). Afferent impulses from the cardiovascular receptors exert a tonic inhibition of the ADH release by acting upon its final neuronal link (the cells of the supraoptic and paraventricular nuclei). Afferent inflow from these receptors also inhibits thirst to some extent, perhaps by preventing at some synaptic level information from cerebral "thirst" sensors from reaching other parts of the brain where the information is converted into a conscious urge to drink. Therefore, increased cardiovascular receptor activity becomes manifested as elevated osmotic thresholds for ADH liberation and thirst. Severe volume depletion may induce RAS hyperactivity to such an extent that generated angiotensin II stimulates the ADH release and water intake. Demonstrated cerebral Na/angiotensin interaction suggests that this may occur via an angiotensin-induced lowering of the stimulus threshold for the sensors involved in the osmotic control of water balance. Cerebral damage affecting the sensors responsible for the osmotic regulation of water intake and ADH release may result in hypo- or adipsia associated with latent diabetes insipidus, and is apparently the ultimate cause of "essential" hypernatremia. This fragmentary outline of the cerebral control of water intake is based to a considerable extent upon circumstantial evidence, and is for that reason speculative on many points.
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PMID:Regulation of water intake. 676 37

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

Rats with electrolytic lesions of the tissue surrounding the third ventricle (AV3V) of the hypothalamus exhibit hypernatremia and chronic drinking deficits in response to hypertonic NaCl. These findings are suggestive of impaired osmoreception. The organ-cultured rat hypothalamo-neurohypophyseal system (HNS) previously has been shown to release vasopressin (VP) in response to osmotic stimuli. The ventral portion of the region damaged by AV3V lesions is included in the HNS explant. Thus, these studies were initiated to evaluate the ability of HNS explants which were obtained from rats previously prepared with AV3V lesions to respond to an increase in osmolality, acetylcholine, or angiotensin II with an increase in VP release. Following electrolytic ablation of the AV3V region or sham lesions and a 2-week recovery period, HNS explants were removed from rats with sham or AV3V lesions. The explants were maintained in organ culture for 4 days. On the third day in culture, increasing the osmolality of the culture medium from 295 to 315 mosm/kg H2O by the addition of NaCl resulted in a 2.5-fold increase in VP release from the explants with sham lesions, but did not significantly alter VP release from the explants with AV3V lesions. On the subsequent day in culture, acetylcholine (10(-5) M) stimulated VP release from the explants with AV3V lesions as well as the explants with sham lesions. Angiotensin II (10-5 M) also stimulated VP release from explants obtained from rats with both AV3V and sham lesions. These data suggest that the osmoreceptors which are involved in controlling VP release from the organ cultured HNS may be located in the region of the AV3V.
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PMID:Effect of anteroventral third ventricle lesions on vasopressin release by organ-cultured hypothalamo-neurohypophyseal explants. 688 61

A syndrome of chronic hypernatremia (range 148 to 161 mmoles/l) and partial hypopituitarism (growth hormone and gonadotropin deficiencies) is reported in a 27 year-old man with sarcoid hypothalamic involvement. The patient did not complain of thirst and spontaneous fluid intake was not sufficient to restore the serum sodium to normal. However, when larger amounts of water were given (50 ml/kg for 180 min), the plasma osmolality returned to normal values in 3 hours. Blood volume values were found subnormal on two occasions on free diet (63 and 74% of the theorical normal values) and plasma renin activity was elevated (22 ng/ml/hour). Plasma vasopressin (AVP) concentrations (range < 1 to 1.9 pg/ml) were inappropriately low for the degree of plasma osmolality and remained markedly subnormal when hypertonic saline was infused (NaCl 5%, 10 ml/min for 60 min). However, the secretory stores and hemodynamic control of AVP release were intact since a rise in plasma AVP to 10.8 pg/ml was observed after induction of arterial hypotension with sodium nitroprusside infusion. These results provide further direct evidence fo the dysfunction of the thirst mechanism and the osmotic contol of AVP release. They support the concept that osmoreceptor areas are anatomically distinct from the neurohypophyseal AVP secretory system and that neural inputs from baroreceptor and osmoreceptor cells are completely separated.
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PMID:Chronic hypernatremia, hypovolemia and partial hypopituitarism in sarcoidosis: a case report. 699 62

Investigations in a 14 year old girl with arrested growth for 2 years, delayed pubertal development, hypernatraemia without thirst, diabetes mellitus and hyperlipaemia are reported. The hypernatraemia was accompanied by a low vasopressin concentration with an abnormal response to thirst, high plasma renin but normal plasma aldosterone concentrations. Treatment with vasopressin and increased fluid intake decreased serum sodium levels. Serum gonadotrophins were low; GH response during an insulin tolerance test was subnormal and basal serum Prl concentration was elevated. Bone age, thyroid function and adrenal function were normal. After initiation of bromocriptine treatment her growth accelerated and regular menstruations commenced. The serum gonadotrophin levels increased and showed pulsatile release. A hypothalamic disorder is suggested, but no cerebral lesion could be demonstrated.
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PMID:Hypernatraemia, diabetes mellitus, hyperprolactinaemia, retarded growth and delayed puberty in a 14 year old girl. Effect of bromocriptine treatment. 700 94

The osmolality of body fluids is normally maintained within a narrow range. This constancy is achieved largely via hypothalamic osmo-receptors that regulate thirst and arginine vasopressin, the antidiuretic hormone (ADH). Anything that interferes with the full expression of either osmoregulatory function exposes the patient to the hazards of abnormal increases or decreases in plasma osmolality. Hyposmolality is almost always due to a defect in water excretion. Increased intake may contribute to the problem but is rarely, if ever, a sufficient cause. Impaired water excretion can be due to a primary defect in the osmoregulation of ADH (inappropriate antidiuresis) or secondary to nonosmotic stimuli like hypovolemia or nausea. The two types differ in clinical presentation and treatment. Resetting of the ADH osmostat is commonly associated with resetting of the thirst osmostat. Hyperosmolarity is almost always due to deficient water intake. Excessive excretion may contribute to the problem but is never a sufficient cause. Impaired water intake can result from a defect in either the osmoregulation of thirst of the necessary motor responses. Thirst may be deficient because of primary osmoreceptor damage as in the syndrome of adipsic hypernatremia or secondary to nonosmotic influences on the set of the system. They are distinguishable by the clinical presentation as well as the type of ADH defects with which they are associated. So-called essential hypernatremia due to primary resetting of the osmostat has been postulated, but unambiguous evidence for such an entity has not yet been reported.
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PMID:Neurogenic disorders of osmoregulation. 703 30


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