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)

Hyponatremia is a common disorder. When hyponatremia is the result of hypothyroidism it can be successfully treated with thyroid hormone substitution. We followed cumulative sodium- and fluid balances of a patient with hyponatremia, resulting from hypothyroidism. We concluded that hyponatremia in hypothyroidism is due to a pure renal mechanism, and cannot be ascribed to inappropriate secretion of antidiuretic hormone.
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PMID:Hyponatremia due to hypothyroidism: a pure renal mechanism. 1124 14

Perioperative hyponatremia has been recognized as a serious in-hospital complication for many years. Because the kidney responds to changes in extracellular fluid tonicity by adjusting water excretion, a defect in any of several key elements of water excretion can lead to water retention and hyponatremia. Most cases of hyponatremia are caused by impaired renal water excretion in the presence of continued water intake. For the kidney to excrete excess free water and thereby protect the extracellular fluid against hyponatremia, there must be an adequate glomerular filtration rate (GFR), adequate delivery of glomerular filtrate to the diluting segments of the distal nephron, intact tubular diluting mechanisms, and appropriate inhibition of antidiuretic hormone (ADH) synthesis and release. Virtually all of the clinical disorders producing hyponatremia are based on abnormalities of these few mechanisms of water regulation. Finding the reason for impaired renal water excretion is the key to diagnosing the cause of hyponatremia. Impaired renal water excretion may be caused by impaired GFR (renal failure), impaired water delivery to the diluting segments of the distal nephron because of increased proximal reabsorption (decreased extracellular fluid volume and edematous states), impaired renal diluting mechanism (thiazide diuretics), the syndrome of inappropriate ADH (SIADH) due to a variety of causes including the perioperative state, and hypothyroidism or adrenal insufficiency. Any of the states that impair water excretion can produce hyponatremia in a patient with an initially normal serum sodium concentration if sufficient free water is supplied. Therefore, a patient who has one of the conditions listed above, including the perioperative state, may be considered "water intolerant" even if the serum sodium is normal. Such a patient is at risk for developing severe hyponatremia if given hypotonic IV fluids or a large oral water load. An understanding of the basic mechanisms leading to impaired water excretion and "water intolerance" is therefore an important key to avoiding perioperative hyponatremia.
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PMID:University of Miami Division of Clinical Pharmacology Therapeutic Rounds: the water-intolerant patient and perioperative hyponatremia. 1131 70

Central diabetes insipidus is clinically masked in dialysis patients. We report a 12-year-old girl receiving a living-related donor graft for renal failure from Alport syndrome, in whom a craniopharyngioma had been resected 6 months before transplantation. Pretransplant evaluation had documented central hypothyroidism, growth hormone deficiency, and presumptive hypogonadotropic hypogonadism. The corticotropin-releasing factor test had been normal. Four hours after transplantation, urine output exceeded 1,000 ml/h without diuretic therapy. Serum sodium concentration was 155 mmol/l, serum osmolality 333 mmol/kg, and plasma antidiuretic hormone 4.9 ng/l, while urine osmolality was 233 mmol/kg. Desmopressin acetate was started by continuous intravenous infusion at 1 microgram/day. Serum electrolytes rapidly normalized, urine output stabilized at 2 l/day. The patient was discharged 4 weeks after transplantation with good allograft function, receiving intranasal desmopressin acetate 10 micrograms twice daily. Pre-existing central diabetes insipidus is unmasked after successful kidney transplantation, leading to rapid dehydration and hypernatremia, which can be prevented by prompt institution of desmopressin therapy.
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PMID:Perioperative management of central diabetes insipidus in kidney transplantation. 1135 73

OBJECTIVES: This study was undertaken to investigate the effects of hypovolemic and hypertonic treatments on plasma vasopressin (AVP) levels and fluid balance in thyroidectomy-induced hypothyroidism in the rat. The influence of hypothyroidism on AVP responsiveness to hypertonic and hypovolemic stimuli were compared. MATERIALS & METHODS: Adult male rats were divided into two groups. The rats were surgically thyroidectomized (hypothyroid) or sham-operated (euthyroid). Two weeks later these groups were further divided in three subgroups each containing six rats. The first subgroup consisted of unchallenged rats. The second group underwent hypovolemic treatment by using I.P. 700 mg polyethylene glycol. The third subgroup consisted of hypertonic (1.5 M NaCl; 1 ml/100 g) stimulated animals. All rats were decapitated and trunk blood collected in heparinized tubes. Plasma samples were stored at -20 degrees C until assayed. Plasma AVP, T3 and T4 levels were measured by radioimmunoassay. Hematocrit values and plasma Na and K concentrations were also determined. RESULTS: In the hypothyroid rats, hypovolemic treatment significantly reduced the expected increases in plasma AVP levels (p<0.05) compared to the respective intact animals. In the hypertonic group, similar increases occurred in plasma AVP levels of hypothyroid and euthyroid rats. Hematocrit values and plasma Na concentrations were not significantly different in the hypothyroid rats compared to euthyroid rats. CONCLUSION: In conclusion, thyroidectomy-induced hypothyroidism may affect AVP response to hypovolemic stimulus although it has no important effect on basal AVP levels nor AVP response to hypertonic stimulus.
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PMID:Influence of hypovolemic and hypertonic treatments on plasma vasopressin levels and fluid balance in the thyroidectomy-induced hypothyroid rats. 1145 27

This study was undertaken to investigate the effects of hypovolemic and hypertonic treatments on plasma vasopressin (AVP) levels and fluid balance in propylthiouracil (PTU)-induced hypothyroidism in the rat. The influence of hypothyroidism on AVP responsiveness to hypertonic and hypovolemic stimuli were compared. Adult male rats were divided into two groups. Groups I and II were intraperitoneally (i.p.) injected with saline (1ml/250g) and PTU (10mg/kg/day), respectively, for a period of two weeks. These groups were further divided in three subgroups each containing six rats. The first subgroup consisted of unchallenged rats. I.P. 700 mg polyethylene glycol was used for hypovolemic treatment. The third subgroup consisted of hypertonic (1.5 M NaCl; 1ml/100 g) stimulated animals. All rats were decapitated and trunk blood collected in hep-arinized tubes. Plasma samples were stored at -20 degrees C until assayed. Plasma AVP, T3 and T4 levels were measured by radioimmunassay. Hematocrit values and plasma Na concentrations were also determined. In the PTU-induced hypothyroid rats, hypertonic treatment caused lower increase in plasma AVP levels (p<0.05) compared to the respective control animals. In the hypovolemic group, decreases in AVP responses were not found to be statistically significant. In conclusion, although hypothyroidism does not statistically change basal AVP levels, it may affect AVP response to hypertonic stimulus. It is not clear whether changes in fluid-electrolyte balance cause disturbance in AVP release in hypothyroidism or vice versa. Therefore, these preliminary findings need to be confirmed by further investigations.
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PMID:Influence of hypovolemic and hypertonic treatments on plasma vasopressin levels and fluid balance in the propylthiouracil-induced hypothyroid rat. 1146 93

Hyperthyroidism or hypothyroidism are commonly associated with altered blood pressure (BP). Restriction of sodium in the diet produces a decrease in BP in some individuals. It is also well known that hormones other than thyroid affect BP. The present study was designed to evaluate the influence of a low sodium diet on BP in patients with hyperthyroidism or hypothyroidism during therapy. The occurrence of salt-sensitive or salt-nonsensitive BP was compared with hormonal levels (plasma renin activity, aldosterone, atrial natriuretic peptide, and arginine vasopressin). Patients with hyperthyroidism (75 subjects) were investigated before the initiation of treatment, 2 weeks after the treatment, and after the attainment of euthyroid state. Patients with hypothyroidism (31 subjects) were studied before the treatment and in the euthyroid state. Control values were obtained from 37 healthy individuals. Blood pressure, changes of plasma volume, serum aldosterone, atrial natriuretic peptide, vasopressin levels, and plasma renin activity were measured in all investigated subjects after application of a normal sodium diet and after 3 days on a low sodium diet. Elevated systolic BP was found in patients with hyperthyroidism and hypothyroidism. Mean arterial BP was higher only in the untreated hypothyroid patients. The high incidence of salt-sensitive BP was found only in untreated hypothyroid patients. Also in hypothyroid patients the application of a low sodium diet led to a lower increase in plasma renin activity in subjects with salt-sensitive BP than in individuals with salt-resistant BP. Therefore, different mechanisms are responsible for BP elevation in patients with hyperthyroidism or hypothyroidism.
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PMID:Influence of short-time application of a low sodium diet on blood pressure in patients with hyperthyroidism or hypothyroidism during therapy. 1171 Jul 92

The syndrome of inappropriate antidiuretic hormone (SIADH), the most common cause of euvolemic hyponatremia, is due to nonphysiologic release of arginine vasopressin from the posterior pituitary. Hyponatremia induced by SIADH can be caused by several conditions, such as central nervous system disorders, malignancies, various nonmalignant lung diseases, hypoadrenalism, and hypothyroidism. A 67-year-old man developed hyponatremia consistent with SIADH. Although common comorbid conditions associated with SIADH were excluded as possible causes, his medical history and drug regimen were extensive. However, he had been taking spironolactone, amiodarone, and simvastatin for less than 3 months. Amiodarone was discontinued based on a case report suggesting that this drug can cause SIADH-induced hyponatremia. The patient's serum sodium level began to rise within 3 days of discontinuation and returned to normal within 1 month. Although SIADH-induced hyponatremia occurs only rarely, it should be recognized as a possible adverse effect of amiodarone.
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PMID:Syndrome of inappropriate antidiuretic hormone-induced hyponatremia associated with amiodarone. 1201 66

Hypothyroidism is associated with significant abnormalities in the renal handling of salt and water. To address the involvement of tubular transport proteins in these abnormalities, rats were rendered pharmacologically hypothyroid and the abundance of major tubular transport proteins was assessed by immunoblot and immunohistochemistry. Hypothyroidism resulted in a marked reduction in kidney size and creatinine clearance along with decreased or unchanged total kidney abundance of the transport proteins. Whereas the proximal tubular type 3 Na/H exchanger (NHE3) and type 2 Na-phosphate cotransporter (NaPi2) stood out by their disproportionately reduced abundance, the bumetanide-sensitive type 2 Na-K-2Cl cotransporter (NKCC2) and aquaporin-2 (AQP2) were unaltered in their total kidney abundance despite a markedly lower kidney mass. The latter proteins in fact showed enhanced immunostaining. Decreased NHE3 and NaPi2 expression was most likely due to a combination of triiodo-l-thyronine (T(3)) deficiency along with a reduced glomerular filtration rate. The increased abundance of NKCC2 and AQP2 may have been caused by an increased action of vasopressin since urinary excretion of this hormone was elevated. On the other hand, the thiazide-sensitive Na-Cl cotransporter; the alpha-, beta-, and gamma-subunits of the amiloride-sensitive epithelial Na channel; and the alpha(1)-subunit of Na-K-ATPase showed a moderate decrease in total kidney abundance that was largely proportional to the smaller kidney mass. Although the observed expression of transporters was associated with a balanced renal sodium handling, altered transporter abundance may become functionally relevant if the hypothyroid kidney is challenged by an additional destabilization of the milieu interieur that has previously been shown to result in an inadequate natriuresis and clinical symptoms.
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PMID:Renal expression of sodium transporters and aquaporin-2 in hypothyroid rats. 1256 81

Hypothyroidism is associated with impaired urinary concentrating ability in humans and animals. The purpose of this study was to examine protein expression of renal sodium chloride and urea transporters and aquaporins in hypothyroid rats (HT) with diminished urinary concentration as compared with euthyroid controls (CTL) and hypothyroid rats replaced with L-thyroxine (HT+T). Hypothyroidism was induced by aminotriazole administration. Body weight, water intake, urine output, solute and urea excretion, serum and urine osmolality, serum creatinine, 24-h creatinine clearance, and fractional excretion of sodium were comparable among the three groups. However, with 36 h of water deprivation, HT rats demonstrated significantly greater urine flow rates and decreased urine and medullary osmolality as compared with CTL and HT+T rats at comparable plasma vasopressin concentrations. Western blot analyses revealed decreased renal protein abundance of transporters, including Na-K-2Cl, Na-K-ATPase, and NHE3, in HT rats as compared with CTL and HT+T rats. Protein abundance of renal AQP1 and urea transporters UTA(1) and UTA(2) did not differ significantly among study groups. There was however a significant decrease in protein abundance of AQP2, AQP3, and AQP4 in HT rats as compared with CTL and HT+T rats. These findings demonstrate a decrease in the medullary osmotic gradient secondary to impaired countercurrent multiplication and downregulation of aquaporins 2, 3, and 4 as contributors to the urinary concentrating defect in the hypothyroid rat.
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PMID:Urinary concentrating defect in hypothyroid rats: role of sodium, potassium, 2-chloride co-transporter, and aquaporins. 1259 91

Anorexia nervosa is a syndrome with multifactorial etiology in which several genetic, biologic, psychological and social factors are involved. Patients affected by anorexia nervosa (AN) may develop multiple endocrine abnormalities, e.g. amenorrhea, hypothalamus-pituitary-adrenal axis hyperactivity, low T3 syndrome and peculiar changes of somatotroph axis function. These endocrine abnormalities are also found after prolonged starvation and may represent an adaptive response developed in order to save energy and proteins. It is still a matter of debate whether these endocrine changes are etiologic or secondary. In fact, several evidences suggest the existence in AN of hypothalamus functional alterations, which may be involved in the development and maintenance of the food intake disorder; on the other hand, the increased CRH secretion seems to be secondary to malnutrition as well as GH hypersecretion coupled to low IGF-I levels; the latter is a common finding in AN, as well as in other undernutrition and malabsorption conditions, type 1 diabetes mellitus, liver cirrhosis and catabolic states. Hypothalamic amenorrhea, which is one of the diagnostic criteria for AN, is not linked only to the reduction of body weight but reflects also deep alterations of gonadotropin secretory pattern. Low T3 syndrome is frequently found in AN; on the other hand, an iodide-induced hypothyroidism is quite uncommon. T3 reduction in AN seems to be an adaptive response to prolonged starvation; however the presence of a simultaneous central dysregulation cannot be excluded. Finally, AN patients frequently show defects in urinary concentration or dilution with inappropriate secretion of antidiuretic hormone, which may be due to intrinsic defects in the neurohypophysis or to abnormalities of its regulatory afferent neurons.
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PMID:[Endocrine abnormalities in anorexia nervosa]. 1271 47


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