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)

This study has been done to evaluate serum calcium, phosphorus (P), magnesium, parathyroid hormone (PTH), calcitonin (CT), and cyclic adenosine monophosphate (cAMP) in recently diagnosed pulmonary tuberculous patient, (n = 61) and the results were compared with the healthy control group (n = 22). Twenty four hours urine was collected for estimation of these electrolytes as well as cAMP. Nephrogenous cAMP (NcAMP) was calculated. Serum Ca and PTH were significantly reduced in TB groups, but CT was elevated. Serum Mg, P and cAMP as well as urinary Ca and Mg in TB groups were similar to that of the control group. Urinary P, cAMP NcAMP were increased in patient groups compared with the control. The reduced serum Ca could be due to impaired intestinal absorption of Ca, or deficient intake as a result of anorexia, decreased plasma albumin, decreased active metabolites of vitamin D or elevated CT. The rise in serum CT in TB might be due to increased CT secreted from the bronchial K-cells. Increased NcAMP might be due to the associated increase in serum antidiuretic hormone (ADH). The elevated urinary P in TB could be attributed to tissue breakdown, decreased serum PTH or increased CT.
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PMID:Calcium homeostasis in untreated pulmonary tuberculosis. I--Basic study. 216 2

The effects of chronic phosphate depletion on vasopressin (ADH) secretion and kidney tissue ADH concentration were examined in rats fed on a diet containing 0.26% phosphorus (LP) or 0.99% phosphorus (NP). The concentration of plasma phosphorus (P) fell significantly in the LP rats after a 4-week period on the experimental diet. There was no significant difference between the LP and NP rats as regards their plasma ADH concentrations and kidney tissue ADH concentrations in normal hydration after a 4-week period on the experimental diets. Following hypertonic saline tests, the plasma ADH concentrations increased significantly in the LP and NP rats, but there was no significant difference between the groups. The kidney medulla and papilla ADH concentrations increased significantly with plasma ADH elevations in both groups. Again, no difference could be found in the cortico-medullary ADH concentration gradients between the two groups. These results indicate that chronic hypophosphatemia in phosphate depleted rats may not be related to ADH secretion and the distribution or tissue concentration of ADH in the kidney. Further, our data suggest that a low plasma P does not influence the ability of ADH to bind to kidney receptor in rats.
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PMID:Effect of phosphate depletion on vasopressin secretion and kidney tissue vasopressin concentration in rats. 235 63

The effects of atrial natriuretic peptide (ANP) were investigated in six healthy male volunteers taking a constant diet (120 mmol sodium and 60 mmol potassium daily). They were given an intravenous bolus of 100 micrograms human alpha-ANP on one day or placebo on another day 1-3 weeks apart in a double-blind randomised study. After ANP, urinary sodium excretion increased four-fold, and urine volume, calcium, magnesium, and phosphorus excretion doubled within 30 min of the injection. ANP induced an immediate fall in arterial pressure, followed by a longer vasodepressor phase which exceeded the duration of the effect on electrolyte excretion. There were no significant changes in plasma renin activity, aldosterone, antidiuretic hormone, or noradrenaline when compared with placebo.
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PMID:Renal, haemodynamic, and hormonal effects of human alpha atrial natriuretic peptide in healthy volunteers. 285 1

We report two infants with pseudotumor cerebri associated with renal disease. The pathogenesis of increased intracranial pressure in this clinical setting is unclear, but may be mediated by one or more of the conditions commonly associated with pseudotumor cerebri, including sinus thrombosis, increased intravascular fluid volume, anemia, and endocrine disturbances resulting in abnormal calcium and phosphorus metabolism. The onset of pseudotumor cerebri also may be related to changes in vasopressin levels that affect brain water permeability.
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PMID:Pseudotumor cerebri associated with obstructive nephropathy. 350 95

The syndrome of tumor-induced osteomalacia has been previously thought to occur only in association with mesenchymal tumors, although one report has linked prostatic carcinoma with the syndrome. We report the case of a patient who presented first with the clinical and biochemical features of the syndrome of inappropriate antidiuretic hormone secretion, and then oncogenic osteomalacia. The first syndrome was characterized by headaches, nausea, and vomiting; serum sodium determinations ranged between 107 and 118 meq/L with simultaneous urine spot sodium concentrations of 100 to 116 meq/L. The circulating antidiuretic hormone level was markedly elevated to 261.5 microU/mL. The osteomalacia was discovered incidentally when depressed serum phosphorus levels of 1.2 to 1.7 mg/dL were noted in association with 24-hour urine phosphorus excretion exceeding 1000 mg/24 h. Undecalcified tetracycline-labeled bone biopsy samples confirmed oncogenic osteomalacia. Only afterward was a small-cell carcinoma of the lung identified as the likely source of both of these syndromes.
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PMID:Oncogenic osteomalacia and inappropriate antidiuretic hormone secretion due to oat-cell carcinoma. 609 61

A decrease in extracellular pH is well known to inhibit vasopressin stimulated water flow in the toad bladder. It remains unclear whether this inhibition is the result of the effect of extracellular pH per se or the consequence of altered intracellular pH. In the present study we evaluated the effect of several maneuvers capable of altering intracellular pH on vasopressin or cyclic AMP stimulated water flow in the toad bladder in the absence of alterations of extracellular pH. In the presence of a normal extracellular pH, bladders subjected to a high partial pressure of CO2 or bladders from acidotic toads had a significant decrease in vasopressin or cyclic AMP stimulated water flow as compared to controls. We also examined the effect of maneuvers capable of increasing intracellular pH on vasopressin and cyclic AMP stimulated water flow. Intracellular alkalosis was induced by exposing the bladders in vitro to NH4Cl at pH 8 or to acetazolamide. Both maneuvers resulted in a significant decrease in vasopressin, but not in cyclic AMP stimulated water flow. Bladders removed from alkalotic toads, incubated in a normal extracellular pH also showed a decrease in AVP stimulated water flow. Intracellular muscle pH assessed with phosphorus nuclear magnetic resonance, was not different among bladders from control, acidotic and alkalotic toads. It is concluded that alterations of intracellular pH, in the absence of alterations of extracellular pH, are important in regulation of water transport in the toad bladder in response to vasopressin or cyclic AMP. In addition, metabolic acidosis or alkalosis alters AVP or cyclic AMP stimulated water flow by a mechanism independent of the intracellular pH.
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PMID:Acid-base metabolism, intracellular pH and water transport by the toad bladder. 631 61

The role of prostaglandins in the regulation of sodium and water excretion has been widely studied, but little is known about the influence of prostaglandins (PGs) on the tubular handling of calcium, magnesium or phosphorus. Recent observations have suggested that PGE2 and vasopressin may interact and influence reabsorption of calcium and phosphorus in the cortical collecting duct. The present study investigated the effect of meclofenamate (2 mg/kg), and inhibitor of PG synthesis, on the excretion of calcium, magnesium and phosphorus. Experiments were performed in antidiuretic and water diuretic rats to examine potential PG-vasopressin interactions on the reabsorption of these ions by renal tubules. In antidiuretic rats given meclofenamate, urine osmolality increased whereas urine flow and the fractional excretion of water, urea, sodium, calcium and magnesium decreased by 30 to 50%. In water diuretic animals, urine osmolality and urea excretion were unaltered after meclofenamate administration. Fractional excretion of sodium, water, calcium and magnesium declined approximately 50% in water diuretic rats given meclofenamate. Urinary excretion of PGE2 was not significantly different in water diuretic and antidiuretic rats averaging 262 +/- 78 vs. 167 +/- 35 pg/min, respectively. Meclofenamate significantly reduced urinary excretion of PGE2 in both groups. The results indicate that renal PGs modulate renal tubular reabsorption of calcium and magnesium, as well as sodium and water.
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PMID:Prostaglandin-vasopressin interactions on the renal handling of calcium and magnesium. 658 91

In the absence of ADH, microperfused cortical collecting tubules of rabbits reabsorb calcium and phosphorus. Antidiuretic hormone (ADH) (200 microunits/ml Pitressin or synthetic arginine vasopressin) inhibits the reabsorption and may promote the secretion of calcium and phosphorus. At 5 min after incubation with ADH, there was a transitory increase in the potential difference and the reabsorption of sodium. The fluxes of calcium and phosphorus, however, showed no significant change from the control values. At 30-50 min after treatment with ADH, the reabsorption of calcium and phosphorus was inhibited and in some tubules calcium and phosphorus were secreted. The removal of vasopressin from the bath or the addition of 10(-5) M meclofenamate in vitro prevented ADH from inhibiting the reabsorption of calcium and phosphorus. Treatment of tubules with 10(-5) M prostaglandin E2 (PGE2) subsequent to incubation in a medium containing ADH and meclofenamate inhibited the reabsorption or even promoted the secretin of calcium and phosphorus, as did the prolonged incubation with ADH alone. We conclude that cortical collecting tubules reabsorb calcium and phosphorus in the absence of vasopressin and that ADH inhibits calcium and phosphorus reabsorption. Endogenous synthesis of PGE2 may mediate the inhibitory action of ADH, since meclofenamate (an inhibitor of the synthesis of prostaglandins) opposes and exogenous PGE2 mimics ADH.
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PMID:ADH-PGE2 interactions in cortical collecting tubule. II. inhibition of Ca and P reabsorption. 694 97

Rat liver plasma membranes were incubated in Ca2+-free buffer plus 0.5 mM ethyleneglycol-bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) containing 0.5 mg/ml deoxycholate or 50 mU/ml vasopressin or both compounds. The membrane phospholipids were extracted, separated by two-dimensional chromatography and quantitated by phosphorus analysis. Vasopressin significantly enhanced degradation of phosphatidylinositol in the presence of deoxycholate (21% with deoxycholate alone versus 32% in the presence of vasopressin plus deoxycholate). However, no significant effects of deoxycholate or vasopressin were seen on the degradation of phosphatidylcholine, phosphatidylethanolamine or phosphatidylserine. These results indicate that specific degradation of phosphatidylinositol can be seen after direct addition of vasopressin to a plasma membrane preparation.
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PMID:Direct stimulation of phosphatidylinositol degradation by addition of vasopressin to purified rat liver plasma membranes. 708 19

Plasma catecholamines and vascular response to noradrenaline were studied in phosphate depleted rats. Phosphate depletion was induced in rats by dietary phosphorus deprivation for 6 weeks. Basal plasma concentrations of noradrenaline, adrenaline and dopamine were elevated in phosphate depleted rats compared to pairfed control rats. After exposure to cold (4 degrees C, 45 min) the rise in plasma catecholamines was much more pronounced in phosphate depleted rats. In the isolated perfused rat heart, the uptake of tritiated noradrenaline was unchanged. In the isolated perfused hindlimb preparation the vascular response to noradrenaline, but not to potassium chloride and arginine-vasopressin was significantly diminished in phosphate depleted rats. It is concluded that in phosphate depletion sympathetic activity is elevated and vascular response to noradrenaline diminished.
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PMID:Dysfunction of the adrenergic system in phosphate depleted rats. 717 75


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