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 third case of acquired phosphate diabetes associated with a syndrome of inappropriate secretion of antidiuretic hormone (SIADH), related to a pulmonary tuberculosis, is reported. Renal hypophosphatemia in this patient was caused by the erroneous intake of 1 g doxycycline. It is likely that the selective nephrotoxicity in these 3 patients with SIADH was induced by tetracycline.
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PMID:Tetracycline-induced renal hypophosphatemia in a patient with a syndrome of inappropriate secretion of antidiuretic hormone. 327 77

Four male divers were exposed to an environment of 1 ATA air for 7 d, followed by 7 d of 31 ATA He-O2, and following decompression to a postdive 1 ATA air environment for 3 d. Urine and blood were collected for hormonal measurements. Divided 24-h urine collections were obtained during 3 consecutive d at predive 1 ATA conditions, and at 31 ATA conditions. Two consecutive day collections were obtained at early decompression (31-25 ATA), at late decompression (14-8 ATA), and at postdive 1 ATA. Two blood samples were obtained, at predive 1 ATA, at 31 ATA, and at postdive 1 ATA. Plasma antidiuretic hormone (ADH) concentration decreased about 45% (P less than 0.005), while plasma aldosterone concentration and urinary aldosterone excretion were doubled (P less than 0.005) after the subjects were at 31 ATA. Plasma cortisol concentration and plasma parathyroid hormone concentration were not significantly affected by hyperbaria. Urinary excretion of aldosterone was not significantly different between day (0700-1900) and night (1900-0700) at any time, and both day and night excretion rates were increased at 31 ATA through late decompression (P less than 0.005). Urinary ADH excretion was greater during daytime at predive 1 ATA (P less than 0.005), but not thereafter. Both daytime and nighttime ADH excretion rates were decreased from 31 ATA through late decompression (P less than 0.005). It is concluded that hyperbaria eliminates the circadian release pattern of ADH and that the overall reduction of ADH may contribute to the increased free water clearance observed at hyperbaria. Also, increased parathyroid hormone was not associated with the phosphaturia observed at hyperbaria, but increased aldosterone coexisted with the increased kaliuresis observed.
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PMID:Seadragon VI: a 7-day dry saturation dive at 31 ATA. III. Alterations in basal and circadian endocrinology. 331 55

We evaluated the effects of human calcitonin (hCT) on electrolyte excretion in hormone-deprived rats, that is, in the absence of endogenous parathyroid hormone, antidiuretic hormone, thyrocalcitonin and glucagon, the effects of which might have interfered with those of exogenous calcitonin. Plasma hCT levels, measured by radioimmunoassay, varied from 0 to 32 ng/ml. In these rats, hCT decreased magnesium (Mg) and calcium (Ca) excretion in a dose-dependent fashion. Maximal decreases were observed for hCT plasma concentrations comprised between 3 and 5 ng/ml, and persisted at the highest doses. Sodium, potassium, water, and total solute excretions were constant in the calcitonin concentration range explored. The same was observed for phosphate, except that slight but significant phosphaturia was elicited by the highest doses. Calcium and phosphate infusions to attenuate the fall in plasma Ca and phosphate concentration subsequent to hCT infusion, did not alter the hormonal effect on Ca and Mg excretion. hCT can therefore directly modulate Mg and Ca reabsorption by the kidney at plasma concentrations within the physiological range. The maximal effects on Mg and Ca reabsorption were obtained at plasma concentrations which are generally reached after maximal stimulation of endogenous calcitonin secretion. It is suggested that in rats, endogenous secretion of calcitonin stimulates Ca and Mg renal reabsorption without modification of sodium and phosphate excretion.
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PMID:Modulation by calcitonin of magnesium and calcium urinary excretion in the rat. 399 91

Micropuncture and clearance studies were performed on normal untreated and polyuric lithium chloride treated rats (10-12 days). A persistent hypernatremic state quickly developed in the polyuric lithium treated rats during hydropenia resulting from an increased urinary loss of water over sodium chloride, as the fractional excretion of sodium remained at control levels. Superficial proximal tubule and loop of Henle fluid reabsorption was depressed by 8 and 17%, respectively, in lithium-treated rats during this period. By contrast, water reabsorption in the distal tubule and collecting system was significantly increased in the lithium animals, being 27% of the filtered load compared with 20% in normal rats. These results suggest that the urinary-concentrating defect induced by lithium treatment is due primarily to a depression of proximal tubule and possibly loop of Henle function, and that water reabsorption within the distal nephron may in fact be augmented: thus it is unlikely that the action of antidiuretic hormone is significantly impaired. Marked phosphaturia and hypocalciuria were also noted in the lithium-treated rats.
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PMID:Effect of lithium treatment on rat renal tubule function. Evidence against impaired antidiuretic hormone action. 739 71

We report a case of phosphate diabetes in a patient with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with sarcoidosis. Our patient was affected by systemic sarcoidosis and he fits the criteria of Schwartz for the diagnosis of SIADH. He presented with phosphate diabetes which appeared during demeclocycline (DMC) therapy and persisted for about 1 month from the end of DMC. It constitutes the fourth case of phosphate diabetes induced by tetracycline described in the literature and it is the third case of SIADH associated with sarcoidosis.
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PMID:Demeclocycline-induced phosphate diabetes in a patient with inappropriate ADH secretion and systemic sarcoidosis. 845 Sep 17

Recollection micropuncture study was performed in 11 thyroparathyroidectomized dogs during antidiuresis to determine the effect of continuous vasopressin infusion at 50 mU/kg/h on proximal tubule phosphate and sodium transport. The animals were divided into two groups according to changes in mean arterial blood pressure. In the first group (five dogs) with increased blood pressure and glomerular filtration rate (GFR), mean proximal tubule fluid-to-plasma inulin ratio fell significantly from 1.69 to 1.53, whereas it remained unchanged at 1.60 in the second group (six dogs) with no change in blood pressure. In contrast, mean proximal tubule fluid-to-plasma ultrafilterable phosphate ratio increased consistently in both groups, regardless of blood pressure changes. Since natriuresis as well as phosphaturia were observed in all animals, the sodium effect of vasopressin in the distal nephron must be mainly responsible for the natriuresis. It was concluded that vasopressin, when given in the doses employed, inhibits phosphate transport in the proximal tubule and sodium reabsorption in the distal nephron. An additional effect on proximal tubule sodium reabsorption appears to be related to the rise in blood pressure and GFR secondary to vasopressin administration.
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PMID:The effect of vasopressin on phosphate transport in the proximal tubule of the dog. 1134 82