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)

The hypothalamic-neurohypophyseal system functions to maintain plasma osmolality within narrow limits. It also is an important mechanism in maintaining normal body fluid volume. The system exerts its influence via release or inhibition of vasopressin (antidiuretic hormone, ADH) which acts on the kidney to decrease water excretion. Deficiency of ADH is usually due to hypothalamic-neurohypophyseal lesions (central diabetes insipidus) or insensitivity of the kidney to ADH (nephrogenic diabetes insipidus). These patients, if untreated, have the predictable result of dehydration, hyperosmolality, hypovolemia, and eventual death in severe cases. On the other hand, ADH excess of the syndrome of inappropriate ADH secretion due to a variety of causes promotes water retention, hypoosmolality and hyponatremia which, if untreated, may progress to convulsions, coma, and death. It is obviously important to diagnose accurately these pathologic states of hydration. Not only is initiation of treatment in general dependent upon recognition of the disease, but each type of pathologic hydration state has specific treatment which rewards both patient and physician with effective correction of the problem.
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PMID:Vasopressin: deficiency, excess and the syndrome of inappropriate antiduretic hormone secretion. 10 6

The effects of vasopressin administered by continuous infusion (0.75 and 0.5 mU/m2/minutes) was studied in two groups of three normal and two groups of 5 and 8 malnourished children given 0.5 and 0.3 mU/m2/minute. The following parameters were analyzed: urine volume, osmolality, water reabsorption, PAH, urea and inulin clearances, Na and K urinary excretion. Malnourished children had a urine volume 3 to 5 times higher than the normal groups. Vasopressin increased urine volume initially, but a mild antidiuretic effect followed in the normal groups. In malnourished children with a high CH2O, antidiuresis showed quite important figures with vasopressin. A transient fall in PAH and inulin clearances was observed with vasopressin in both malnourished groups with a mild drop in the normal group. Natriuresis with a higher % of the filtered sodium excretion was observed in the malnourished groups and in normal children with 0.5 mU of vasopressin. These results show that vasopressin had similar effects, but at a different level in the normal and malnourished children that we studied.
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PMID:[Renal function in normal and malnourished children given different doses of vasopressin in continuous infusion]. 46 71

The role of antidiuretic hormone (ADH) in the renal concentration defect and hemodynamic changes in protein malnutrition was evaluated in rats with diabetes insipidus (DI) after 2 weeks of low protein feeding. Free water reabsorptive capacity (TcH2O), glomerular filtration rate (GFR), and renal plasma flow (RPF) were measured in the protein deprived rats and in DI rats fed a normal protein diet. The effect of urea supplementation of the low protein diet on renal concentrating capacity was also evaluated. In addition, the renal hemodynamic response to acute administration of ADH was measured and correlated with changes in plasma renin concentration and renal renin content (RRC). Protein deprivation in DI rats resulted in reduced urine osmolality and urea excretion, differences which were reversed by urea supplementation. Protein deprivation did not affect free water reabsorptive capacity but did reduce GFR and RPF. Acute ADH administration significantly increased GFR and RPF in protein-deprived rats; these changes were associated with a reduction in RRC and release. These results suggest that dietary protein restriction does not directly affect the tubular capacity to generate and reabsorb free water. The hemodynamic changes seen in protein deprivation are not mediated by ADH and may be secondary to increased intrarenal angiotensin II.
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PMID:Renal hemodynamics and urinary concentrating capacity in protein deprivation: role of antidiuretic hormone. 158 Mar 17

Stress ulcers are located in the body and fundic part of the stomach. They occur in the majority of severely ill or injured patients, but only about 10% will bleed. The most effective prophylaxis are measures against the condition giving rise to risk factors as septicaemia, shock and malnutrition. The medical prophylaxis consists of antacids and/or histamine2-blockers. Most bleedings will stop after intensive care and medication with vasopressin particularly if risk factors can be eliminated. Gastric surgery should be the last step in the treatment of bleeding stress ulcers and then we recommend non-resectional surgery as gastric devascularisation or suture ligation of bleeding vessels.
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PMID:Prophylaxis and management of stress ulcers. 286 95

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.
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PMID:Endocrine physiology of electrolyte metabolism. 638 78

The records of 23 children with intrasellar and suprasellar neoplasms were reviewed for the results of endocrine evaluations before and after treatment with surgery, irradiation, and/or chemotherapy. Deficiency of at least one pituitary hormone was present in 13 patients before treatment and in 22 patients after treatment. Growth hormone deficiency, the most common endocrine abnormality in the pretreatment period, was present in 12 of 17 patients before treatment and in 17 of 21 patients after treatment. In the posttreatment period, thyroid-stimulating hormone deficiency was as common as growth hormone deficiency and was found in 17 of 21 patients evaluated. Hypothalamic-pituitary-gonadal dysfunction and deficiencies of adrenocorticotropic hormone and antidiuretic hormone also occurred in both the pretreatment and posttreatment periods, but were less common.
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PMID:Endocrine function in children with intrasellar and suprasellar neoplasms: before and after therapy. 721 82

Sixty children aged from 1 month to 12 years (mean (SD) 3.18 (3.49) years) with acute bacterial meningitis were studied for the incidence, clinical manifestations and outcome of the inappropriate secretion of antidiuretic hormone syndrome (SIADH). Serum sodium levels and osmolality of serum and urine were estimated on admission and on days 3 and 10. SIADH was diagnosed in 22 out of 60 cases (36.7%) on admission and in six of 48 cases (12.5%) on day 3. Hyponatraemia without SIADH, attributed to vomiting and fever, was detected in seven cases (11.7%). Serum sodium levels returned to normal within 48 hours in these cases. Serum osmolality and sodium levels took longer to return to normal values in patients with SIADH. However, none of the cases showed any evidence of SIADH on the 10th day. A significant correlation with SIADH was observed in cases with evidence of severe meningeal inflammation (p < 0.001). The incidence of SIADH was highest with Streptococcus pneumoniae (75%), followed by Haemophilus influenzae (57.1%). Overall mortality was 26.7%, and mortality was significantly higher (p < 0.001) in cases with SIADH, all of whom died during the 1st 72 hours. Ten out of 22 cases (45.4%) with SIADH who survived beyond the 1st 72 hours had an uneventful course even though all of them had biochemical evidence of SIADH on the 3rd day. Mortality was quite high also in children with severe malnutrition (75%) and in those with S. pneumoniae as the aetiological organism (75%).
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PMID:Inappropriate secretion of antidiuretic hormone in acute bacterial meningitis. 767 22

A 59-year-old woman had chronic hyponatremia from inappropriate secretion of antidiuretic hormone (SIADH) and malnutrition after recurrent cholecystitis for 2 months. She developed dysarthria, dysphagia, bilateral ptosis, clonic convulsions and delayed onset Parkinsonian features. Magnetic resonance imaging showed increased signal density in the central pons on T2-weighted images. She was also later diagnosed as having systemic lupus erythematosus (SLE). This case is reported because central pontine myelinolysis (CPM) developed in chronic hyponatremia without correction, and manifested with atypical, delayed-onset Parkinsonian features. The patient recovered well from her neurological illness, unlike the poor outcome in previously reported cases of CPM. In addition, the coincidence of CPM and SLE has not, to knowledge, been reported before.
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PMID:Central pontine myelinolysis in chronic hyponatremic patient: a case report. 771 99

Starvation-induced alterations of neuropeptide activity probably contribute to neuroendocrine dysfunctions in anorexia nervosa. For example, CRH alterations contribute to hypercortisolemia and NPY alterations may contribute to amenorrhea. Alterations of these peptides as well as opioids, vasopressin, and oxytocin activity could contribute to other characteristic psychophysiological disturbances, such as reduced feeding, in acutely ill anorexics. Such neuropeptide disturbances could contribute to the vicious cycle that has been hypothesized to occur in anorexia nervosa. That is, the consequences of malnutrition perpetuate pathological behavior.
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PMID:Neuropeptide abnormalities in anorexia nervosa. 873 16

Optic nerve formation in mouse involves interactions between netrin-1 at the optic disk and the netrin-1 receptor DCC (deleted in colorectal cancer) expressed on retinal ganglion cell (RGC) axons. Deficiency in either protein causes RGC pathfinding defects at the disk leading to optic nerve hypoplasia (). Here we show that further along the visual pathway, RGC axons in netrin-1- or DCC-deficient mice grow in unusually angular trajectories within the ventral hypothalamus. In heterozygous Sey(neu) mice that also have a small optic nerve, RGC axon trajectories appear normal, indicating that the altered RGC axon trajectories in netrin-1 and DCC mutants are not secondarily caused by optic nerve hypoplasia. Intrinsic hypothalamic patterning is also affected in netrin-1 and DCC mutants, including a severe reduction in the posterior axon projections of gonadotropin-releasing hormone neurons. In addition to axon pathway defects, antidiuretic hormone and oxytocin neurons are found ectopically in the ventromedial hypothalamus, apparently no longer confined to the supraoptic nucleus in mutants. In summary, netrin-1 and DCC, presumably via direct interactions, govern both axon pathway formation and neuronal position during hypothalamic development, and loss of netrin-1 or DCC function affects both visual and neuroendocrine systems. Netrin protein localization also indicates that unlike in more caudal CNS, guidance about the hypothalamic ventral midline does not require midline expression of netrin.
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PMID:Altered midline axon pathways and ectopic neurons in the developing hypothalamus of netrin-1- and DCC-deficient mice. 1055 99


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