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 79-year-old man was admitted because of consciousness disturbance on August 9, 2002. He had been diagnosed as having chronic myeloid leukemia in 1999, and since then, he had continued to take hydroxyurea (1500 mg/day) orally. On admission, his serum sodium concentration was as low as 119 mEq/L, while urinary sodium excretion was high. Based on the blood picture and lack of hepatosplenomegaly, we considered that the leukemia was still in the chronic phase. Because of normal blood level of the antidiuretic hormone (ADH) concentration and sufficient urine volume, the syndrome of inappropriate ADH secretion (SIADH) was unlikely, and sodium-losing nephropathy was suspected. After discontinuation of hydroxyurea, the urinary sodium excretion decreased and the patient's consciousness became clear concomitantly with improvement in the serum Na level. This patient appears to be the first case of hyponatremia caused by hydroxyurea.
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PMID:[Severe hyponatremia with consciousness disturbance caused by hydroxyurea in a patient with chronic myeloid leukemia]. 1510 40

Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy reserved for use in persistent cases. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.
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PMID:Management of hyponatremia. 1516 58

Renal resistance to vasopressin has been demonstrated in type 1 diabetes and in type 2 diabetes with nephropathy. However, renal response to vasopressin in type 2 diabetes without nephropathy has not been studied. We studied 10 subjects with poorly controlled type 2 diabetes (PCDS; Hb A(1c) >9%), 10 subjects with well-controlled type 2 diabetes (WCDS; Hb A(1c) <7%), and 10 matched nondiabetic control subjects (NDCS) during a euglycemic 8-h water deprivation test. None of the subjects had nephropathy. Water deprivation caused similar rises in plasma vasopressin concentrations in all three groups, but the rise in urine osmolality in PCDS (280.3 +/- 49.7 to 594.4 +/- 88.5 mosmol/kgH(2)O) was lower than in WCDS (360.7 +/- 142.8 to 794.1 +/- 77.3 mosmol/kgH(2)O, P < 0.001) or NDCS (336.0 +/- 123.3 to 786.5 +/- 63.3 mosmol/kgH(2)O, P = 0.019). Total urine output was higher in the PCDS than in WCDS and NDCS (P < 0.05). Linear regression analysis showed that, in PCDS, the osmotic thresholds for thirst (291.9 +/- 4.6 mosmol/kgH(2)O) and vasopressin release (291.1 +/- 2.9 mosmol/kgH(2)O) were higher compared with WCDS (286.6 +/- 1.8 and 286.0 +/- 3.6 mosmol/kgH(2)O, respectively) and NDCS (286.0 +/- 2.4 and 284.1 +/- 4.7 mosmol/kgH(2)O, respectively) (between groups P < 0.001 for both variables). Under conditions of euglycemia, PCDS have impaired renal response to vasopressin and elevated osmotic threshold for thirst and vasopressin release in response to dehydration. Under conditions of chronic hyperglycemia, these abnormalities may significantly contribute to the development of dehydration in PCDS.
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PMID:Attenuation of vasopressin-induced antidiuresis in poorly controlled type 2 diabetes. 1529 31

The contributions to our present knowledge and understanding of diabetes insipidus are briefly surveyed. Though a disease presenting with polyuria and thirst had been recognized since Antiquity, it was not until the 17. Century the distinction was made between diabetes insipidus and diabetes mellitus. At the beginning of the 20. Century almost nothing was known about the function of the pituitary. It was generally believed that diabetes insipidus was a renal disease. Two clinical observations in 1912 suggested an association between the hypophysis and diabetes insipidus. This view was supported by the recognition in 1913 that extract of the posterior lobe of the pituitary was effective in diabetes insipidus. Despite much evidence to the contrary, it was assumed that the antidiuretic hormone was produced in the intermediate lobe of the pituitary. Around 1950 it was finally established that 'the posterior lobe hormones' are in fact secreted in the hypothalamus. At the same time the antidiuretic hormone was isolated and synthesized. More recently, progress within genetics has made it possible to characterize in details other rare types of diabetes insipidus.
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PMID:Diabetes insipidus: historical aspects. 1563 96

Puberty is a period of dramatic physiologic changes when children become adults. Chronic kidney disease (CKD), like many disorders, may delay or blunt the onset and outcomes of puberty. These include attainment of adult height and reproductive capacity. Although nutrition and treatment effects may contribute to these phenomena, increasing evidence supports direct biological effects of CKD on the neurohypophyseal axis that controls these systems. Although CKD affects puberty, this life period also impacts the progression of CKD. Diabetes mellitus, posterior urethral valves, reflux nephropathy, and hypoplasia all appear to accelerate with sexual maturation. Potential mechanisms include increases in blood pressure and body size as well as altered endocrine physiology. Better understanding of the interactions of puberty and CKD may lead to better outcomes for children with CKD as well as longer preservation of native kidney function.
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PMID:Puberty and chronic kidney disease. 1619 76

The mechanism behind iodinated radiocontrast nephropathy remains elusive. Direct oxidative damage is the prevailing hypothesis, but the apparent protective effect of iodine against oxidation contradicts this view. We propose that autonomic dysfunction participates in the pathogenesis of radiocontrast nephropathy and may account for other contrast-associated reactions previously attributed to allergy. Iodine, through its effects on thyroid function and chemoreceptor response to metabolic acidosis, may induce hyperadrenergia and consequently diminish renovascular flow and urine output. The renal response to adrenergia likely served an adaptive function during prehistoric evolution when trauma was a dominant source of hypovolemia and adrenergia, but the response may behave maladaptively today as evolutionarily nai ve triggers for adrenergia have emerged. Autonomic dysfunction can further impair renal function by deranging renovascular autoregulation and inducing oxidative reperfusion injury as a secondary phenomenon. Many other causes of acute renal failure such as drug toxicity, surgery, hospitalization, and diabetes may operate through hyperadrenergia, impaired renovascular autoregulation, and oxidative reperfusion injury. Dialysis, a volume reduction therapy for renal failure, can counterintuitively worsen renal dysfunction by exacerbating adrenergia, which may explain its association with accelerated atherosclerosis, inflammation, and cancer. Other examples of vicious cycles that perpetuate renal dysfunction may include renal artery stenosis, carotid stenosis, and atherosclerosis as well as the cardio-renal, hepato-renal, and pulmonary-renal syndromes. The benefits of hydration and bicarbonate in protecting renal function may operate in part through baroreceptor- and chemoreceptor-mediated reduction of sympathovagal ratio, respectively. New treatment paradigms for renal failure including pharmacologic and electro-mechanical therapies are envisioned based on autonomic remodeling, reduced sympathovagal ratio, and neuromodulation of pathways typically associated with trauma such as renin, angiotensin, vasopressin, and aldosterone.
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PMID:Contrast nephropathy may be partly mediated by autonomic dysfunction: renal failure considered as a modern maladaptation of the prehistoric trauma response. 1633 Jan 57

Hyponatremia, the most common electrolyte disorder, occurs frequently in older people and in hospitalized patients. Physiological changes of aging that interact with diseases and drugs commonly present in older people put this population at greater risk for hyponatremia. It can accompany central nervous system disorders, pulmonary and renal disease, cancer, congestive heart failure, and liver cirrhosis, as well as many commonly used drugs. Delayed recognition can lead to symptomatic hyponatremia with consequent cerebral edema and possibly irreversible neurological damage. Symptoms and signs of hyponatremia may be subtle or not attributed to hyponatremia. Most cases are of the euvolemic type, in which extracellular fluid volume is normal and is often due to the syndrome of inappropriate secretion of antidiuretic hormone. Hyponatremia can also occur in association with hypervolemia or hypovolemia. Common to all of these circumstances is increased secretion of arginine vasopressin (AVP). Understanding of the pathophysiological basis of hyponatremia and of brain compensatory mechanisms is critical to safe treatment. Fluid restriction or infusion of hypertonic saline can improve symptoms and normalize serum sodium levels but does not address excess AVP, which in most cases is the underlying cause of the disorder. A major new approach to treatment of hyponatremia is the development of aquaretics: AVP-receptor antagonists that provide a targeted therapeutic approach to correcting the many kinds of hyponatremia caused by excess AVP levels.
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PMID:Hyponatremia and arginine vasopressin dysregulation: mechanisms, clinical consequences, and management. 1697 Jun 67

Congenital progressive hydronephrosis (cph) is a spontaneous recessive mutation that causes severe hydronephrosis and obstructive nephropathy in affected mice. The mutation has been mapped to the distal end of mouse chromosome 15, but the mutated gene has not been found. Here, we describe the identification of a single base pair change in aquaporin-2 (Aqp2) in cph mutants through genetic linkage mapping. The C-T change led to the substitution of a Ser (S256) by a Leu in the cytoplasmic tail of the Aqp2 protein, preventing its phosphorylation at S256 and the subsequent accumulation of Aqp2 on the apical membrane of the collecting duct principal cells. The interference with normal trafficking of Aqp2 by this mutation resulted in a severe urine concentration defect. cph homozygotes demonstrated polydipsia and produced a copious amount of hypotonic urine. The urine concentration defect could not be corrected by [deamino-Cys1,D-Arg8]-vasopressin (DDAVP, a vasopressin analog), characteristic of nephrogenic diabetes insipidus. The nephrogenic diabetes insipidus symptoms and the absence of developmental defects in the pyeloureteral peristaltic machinery in the mutants before the onset of hydronephrosis suggest that the congenital obstructive nephropathy is most likely a result of the polyuria. This study has revealed the genetic basis for the classical cph mutation and has provided direct genetic evidence that S256 in Aqp2 is indispensable for the apical accumulation, but not the general glycosylation or membrane association, of Aqp2.
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PMID:Congenital progressive hydronephrosis (cph) is caused by an S256L mutation in aquaporin-2 that affects its phosphorylation and apical membrane accumulation. 1664 Oct 94

Mesangial cells are centrally-located glomerular pericytes with contractile, endocrine, and immunity-regulating functions. These cells are thought to maintain normal glomerular function, since mesangial cell proliferation and extracellular matrix formation are hallmarks of chronic glomerular disease. Vasopressin causes mesangial cell contraction, proliferation and hypertrophy. Consequently, the effects of YM218, a potent, nonpeptide vasopressin V(1A) receptor-selective antagonist, on the growth responses of human mesangial cells to vasopressin were investigated. YM218 showed high affinity for vasopressin V(1A) receptors, exhibiting a K(i) value of 0.18 nM. Vasopressin concentration-dependently increased intracellular Ca(2+) levels and induced hyperplasia and hypertrophy in cultured mesangial cells, YM218 potently inhibited these vasopressin-induced responses. These results clearly show that YM218 has both strong affinity for human mesangial cell vasopressin V(1A) receptors and great potency in inhibiting the vasopressin-induced growth responses of mesangial cells controlled by the vasopressin V(1A) receptors. The hyperplasia and hypertrophy of mesangial cells in vitro caused by vasopressin indicate its possible in vivo role in glomerular disease pathogenesis. Therefore, YM218 is a potent pharmacologic probe to investigate the physiologic and pathophysiologic roles of vasopressin in the development of renal disease.
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PMID:Effects of YM218, a nonpeptide vasopressin V(1A) receptor-selective antagonist, on vasopressin-induced growth responses in human mesangial cells. 1667 55

Hepatorenal syndrome is a particular form of functional renal failure which may develop in patients with liver cirrhosis. On a clinical standpoint, precise diagnostic criteria have been established to clearly define this entity, whereas recent advances in the understanding of the biology of vasoactive mediators and the physiology of microcirculation have allowed to better anticipate its pathophysiological mechanisms. During the course of cirrhosis, sinusoidal portal hypertension leads to splanchnic and systemic vasodilation, responsible for a reduction of effective arterial blood volume. As a result, a state of intense renal vasoconstriction develops, leading to renal failure in the absence of any organic renal disease. At this stage, liver transplantation is the only definitive therapy able to reverse renal dysfunction. In recent years, innovative therapies have shown promise to prolong survival in patients with hepatorenal syndrome, including the administration of analogs of vasopressin (mainly terlipressin), the insertion of transjugular intrahepatic portosystemic shunts and the use of novel techniques of dialysis. On a preventive viewpoint, several simple measures have been shown to reduce the risk of hepatorenal syndrome in cirrhotic patients, including the appropriate use of diuretics, the avoidance of nephrotoxic drugs, the prophylaxis of spontaneous bacterial peritonitis and optimal fluid management in patients undergoing large volume paracentesis.
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PMID:[Hepatorenal syndrome in patients with liver cirrhosis]. 1689 84


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