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

Angiotensin II is dipsogenic, and vasopressin (ADH) regulates renal water excretion. Together, these hormones govern overall mammalian water balance. The Brattleboro rat with inherited diabetes insipidus (DI) lacks ADH and is therefore a convenient model with which to elucidate mechanisms regulating water metabolism. In the present studies, angiotensin II has also been removed from DI rats by the administration of an inhibitor (captopril, SQ 14225; D-2-methyl-3-mercaptopropanoyl-L-proline) of the enzyme which converts angiotensin I, the relatively inert component of the renin-angiotensin system, to angiotensin II, the biologically active substance. SQ 14225 reduced the drinking rates, and after 6 days lowered peripheral plasma aldosterone concentrations were associated with hyperkalaemia. We conclude that the polydipsia of diabetes insipidus partly results from elevated plasma renin activities and angiotensin II concentrations seen in this syndrome. Further, the apparent hypoaldosteronism of DI Brattleboro rats reflects differences in both tissue usage of the steroid and adrenocortical sensitivities associated with polyuria, hyperosmolarity and possibly potassium wasting.
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PMID:Captopril (SQ 14225) depresses drinking and aldosterone in rats lacking vasopressin. 38 37

Hyponatremia with simultaneous renal sodium loss was associated with the inappropriate secretion of antidiuretic hormone in a dog with heartworm disease. Antidiuresis caused expansion of extracellular fluid volume, which induced renal salt wasting and a negative sodium balance. The combination of water retention, salt wasting, and inactivation of intracellular solute contributes to the decrease in serum sodium concentration. Water intoxication due to hypotonicity of body gluids induced anorexia, depression, weakness, and incoordination.
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PMID:Inappropriate secretion of antidiuretic hormone in a dog. 50 Apr 39

Lithium carbonate, useful in the treatment of manic-depressive disorders, can produce nephrogenic diabetes insipidus. The drug, therefore, has been used to facilitate renal waster excretion when severe hyponatremia occurs in the syndrome of inappropriate antidiuretic hormone secretion. Symptomatic dilutional hyponatremia developed in a patient with pulmonary carcinoma whom we treated. Lithium carbonate was administered and renal sodium wasting, hypovolemia, and hypotension occurred. Hyperkalemia was also observed, and since adrenal steroid levels were not decreased, impairment of distal tubular function was suggested. Lithium carbonate blocks antidiuretic hormone effect by decreasing collecting duct cyclic adenosine monophosphate generation. These observations suggest that more generalized inhibitory effects on renal tubular function may also result from its use. An alternative drug, demeclocycline, may be preferable.
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PMID:Severe sodium depletion syndrome during lithium carbonate therapy. 93 81

Acute and chronic effects on the fluid balance of radio-frequency forebrain lesions were studied in the goat. Medial lesions which involved practically the entire anterior wall of the third cerebral ventricle cause persistent loss of thirst and lack of significant antidiuretic hormone (ADH) release in response to hypernatraemia and plasma hyperosmolality. As acute response to such lesions an uncompensated, temporary water diuresis was seen, which rapidly caused pronounced hypernatraemia and hypovolaemia. Lesions extending laterally to encroach upon the supraoptic nuclei resulted in persistent signs of weak, inappropriate ADH secretion (=impaired water diuresis, renal salt wasting, and pronounced hyponatraemia during hydration). Forebrain damage, mainly restricted to the septal region, caused hyperdipsia. In some goats, obvious post-lesioning increase in salt appetite was observed which could not be coreelated to the extent of their forebrain damage. The results are discussed in relation to hypothalamic syndromes in man and previous studies on central control of fluid balance in the goat.
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PMID:Perturbations in fluid balance induced by medially placed forebrain lesions. 118 46

Seventeen unselected, consecutive patients with intracranial disease and accompanying hyponatraemia were studied. All would previously have been diagnosed as having the syndrome of inappropriate antidiuretic hormone (ADH) secretion on the basis of spot plasma/urinary electrolyte testing with the application to them of existing standard laboratory criteria. Timed urinary collections and matching plasma samples were available in all but three cases for the derivation of creatinine, osmotic and free-water clearances, tubular reabsorbed water, and fractional water and sodium excretions. In a number of patients the plasma renin, aldosterone and ADH levels were also assayed. On the basis of the overall findings, 13 patients were diagnosed as in fact having a salt-wasting state whilst in only four patients was the diagnosis of inappropriate ADH secretion (SIADH) substantiated. It is suggested that obtaining simple derived parameters of sodium and water homeostasis can add significantly in differentiating between these quite opposite syndromes.
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PMID:Hyponatraemia in neurosurgical patients: diagnosis using derived parameters of sodium and water homeostasis. 144 68

Two cases with pituitary tumour developed postoperative hyponatraemia which was not caused by inappropriate secretion of antidiuretic hormone. The one case with non-functioning macro-adenoma showed severe hyponatraemia (116 mEq/l) on day 11 after trans-sphenoidal surgery in association with diabetes insipidus (DI). The patients was treated by aqueous pitressin and saline administration to control urinary output and keep positive salt balance at the same time. The other case with GH-producing macro-adenoma showed progressive negative sodium balance with the total loss of 644 mEq resulting in hyponatraemia of 133 mEq/l. This was corrected by additional salt intake. The plasma atrial natriuretic polypeptide (ANP), antidiuretic hormone (ADH) as well as aldosterone levels were normal in the latter case. These patients were considered to manifest primary salt wasting disorder, which should be clearly differentiated from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH).
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PMID:Cerebral salt wasting syndrome distinct from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). 160 86

Subarachnoid hemorrhage induces a lot of extracerebral disturbances such as: systemic hypertension, electrocardiographic abnormalities both morphological, rhythmic and subendocardial damages; those events have been interpreted as overactivity of the sympathetic nervous system. In biochemical changes, hyponatremia early recognized was referred during a long time to a syndrome of inappropriate secretion of antidiuretic hormone. Hyponatremia is now referred to a cerebral salt-wasting. Hypovolemia often observed supports the use of volemic expansion in the prevention and treatment of ischemic complications associated with ruptured intracranial aneurysms. The hypothalamus which lies in close anatomical proximity to the circle of Willis may be directly influenced by the rupture of a cerebral aneurysm. So, hypothalamic dysfunction may affect pituitary adrenal function sympathetic and parasympathetic activities. The knowledge of all these disturbances, and their mechanisms supports the current strategies for the management of aneurysmal subarachnoid hemorrhage.
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PMID:[Physiopathology of meningeal hemorrhage caused by aneurysmal rupture: extracerebral aspects]. 228 35

Hyponatremia, in patients with central nervous system disease, can be attributable to impaired free water excretion (syndrome of inappropriate secretion of antidiuretic hormone) or to excessive sodium excretion (cerebral salt wasting). We present a patient with a parietal glioma and hyponatremia characterized by salt wasting and dehydration. Rehydration and sodium repletion corrected the sodium and volume deficits; withdrawal of supplemental sodium resulted in recurrence of dehydration and hyponatremia. We determined sodium and water balance and measured plasma atriopeptin, antidiuretic hormone, and aldosterone. Plasma atriopeptin ranged from 8 to 44 pg/mL (normal, less than 45 pg/mL); antidiuretic hormone was not elevated at 4 to 5 pg/mL, and aldosterone was slightly elevated at 1040.25 pmol/L. The concentrations of these hormones could not directly explain the natriuresis; interactions with neural or other humoral factors may be involved. In evaluating such patients, careful attention to sodium and water balance is important to guide appropriate therapy.
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PMID:Sodium and water regulation in a patient with cerebral salt wasting. 275 34

Hyponatremia frequently complicates the care of neurosurgical patients and requires prompt effective therapy. These patients commonly fulfill the laboratory criteria of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or cerebral salt wasting; the classification depends on the volume status of the patient. The authors have been dissatisfied with the standard therapy of fluid restriction for the critically ill neurosurgical patient because of 1) slow rates of sodium correction; 2) poor applicability in patients requiring multiple intravenous medications and/or nutritional support; and 3) possible dangers of inducing or enhancing cerebral ischemia in patients who already may be fluid-depleted. Reported successes in the treatment of hyponatremia due to SIADH by administration of urea and normal saline led to the authors' routine use of this therapy for hyponatremic neurosurgical patients. A retrospective review of an 18-month period revealed 48 patients (3% of all neurosurgical inpatients) with hyponatremia from various causes who received 62 treatments of urea and normal saline. Treatment consisted of 40 gm urea dissolved in 100 to 150 ml normal saline as an intravenous drip every 8 hours and an intravenous infusion of normal saline at 60 to 100 ml/hr for 1 to 2 days. The mean pretreatment serum sodium level (+/- standard deviation) was 130 +/- 3 mmol/liter (range from 119 to 134 mmol/liter). There was a significant mean posttreatment elevation to 138 +/- 4 mmol/liter (range 129 to 148 mmol/liter) (p less than 0.001, Student's t-test). Average daily fluid intake and output on treatment days were 2719 +/- 912 and 2892 +/- 1357 ml, respectively. There were no treatment complications in this group. It is concluded that urea and saline administration results in a rapid, safe, and effective correction of hyponatremia, making this method superior to fluid restriction in many neurosurgical patients.
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PMID:Administration of intravenous urea and normal saline for the treatment of hyponatremia in neurosurgical patients. 280 38

Two cases of hyponatremia with intracranial lesions are reported with emphasis on diagnostic value of measurement of antidiuretic hormone (ADH) and atrial natriuretic polypeptide (ANP). Case 1. A 77-year-old female was transferred to our hospital for further care of vegetative state after subarachnoid bleeding on May 23, 1986. She was operated by neck clipping of rt-IC bifurcation aneurysm and lt-internal carotid-posterior communicating aneurysm at another hospital. On admission, computed tomography showed diffuse low density at bilateral thalamus and centrum semiovale. Biochemical analysis revealed hyponatremia (120 mEq/t) with increased natriuresis. Endocrinological date revealed normal plasma ADH and high plasma ANP levels. Patient was treated with infusion of 1% NaCl. Case 2. A 65-year-old male was admitted to our department because of gradual impairment of consciousness and generalized convulsion. Computed tomography showed small low density area at rt-thalamus and lt-cerebellar hemisphere. Biochemical date revealed severe hyponatremia (91 mEq/t) with normal plasma level of ADH and high plasma ANP. He was treated with infusion of 3% NaCl and hyponatremia was improved. The hyponatremia is frequently associated with intracranial disorders such as brain tumor, subarachnoid hemorrhage and head injury. Originally, hyponatremia with natriuresis was thought to be caused by salt wasting. This syndrome was defined as the inability to prevent salt loss in the urine due to undefined natriuretic factor in the brain. However, since 1957, because of introduction of concept of SIADH, it has generally become accepted that patients with natriuresis had SIADH. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hyponatremia with high plasma ANP level--report of two cases with emphasis on the pathophysiology of cerebral salt wasting]. 296 7


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