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 treatment of a patient with diabetes insipidus (DI) is described, and the general treatment of the syndrome is reviewed. The patient was a 16-year-old male who had experienced pain, inflammation and tenderness in the left gluteal region owing to an abcess at the site of intramuscular injection of vasopressin tannate in oil (VTO). (He had been diagnosed as having DI at age 8. Since then, he had been maintained on VTO, lypressin and posterior pituitary snuff.) After the abscess healed during hospital treatment, VTO was stopped and the patient's urinary output increased sharply; urine specific gravity and osmolarity decreased correspondingly. Three days after stopping VTO, the investigational drug, 1-deamino-8-D-arginine vasopressin (DDAVP), was begun at 10 microgram every 12 hours. The dose was eventually increased to 20 microgram every 12 hours, and the patient was discharged on this regimen which controlled his urine output, specific gravity and osmolarity. Other treatments reviewed include antidiuretic-hormone-replacement agents (vasopressin, lypressin) and drugs used to potentiate low ADH levels (chlorpropamide, clofibrate and carbamazepine).
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PMID:Treatment of diabetes insipidus with DDAVP. 90 88

Rabbits immunized with lysine-vasopressin bovine serum albumin conjugate showed the diabetes insipidus syndrome intermittently manifested by polyuria and polydipsia with various degrees of peaking from the eighth to fourteenth day post injection during boosters. The antibody-antidiuretic hormone immune complexes which may interfere with the action of the endogenous vasopressin on the kidney were found in the diabetes insipidus rabbits. However, the degree of the polyuria was not necessarily related to the quantities of the formed immune complexes, the titer, nor the affinity of the antiserum. It is suggested that the degree of the polyuria is related not only to the binding ability of the antiserum to the endogeneous vasopressin, but also to other factors.
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PMID:Immune complexes in diabetes insipidus syndrome of rabbits immunized with vasopressin. 91 33

A 38-year-old physician developed polyuria and hypodipsia four days after the onset of an upper respiratory tract infection. Subsequent investigation showed a concentration defect with dehydration that partially corrected with vasopressin injection (Pitressin) administration compatible with partial central diabetes insipidus (DI). Skull roentgenograms, EEG, and lumbar puncture were normal. The polyuria and hypodipsia slowly resolved without treatment. Normal urinary concentration ability was achieved by the 48th day, but a residual elevation in serum osmolarity persisted for one year. Review of the literature failed to show previous documentation of transient DI with elevated serum osmolarity from an acute, febrile illness. The mechanism is speculative, but may be related to a subclinical encephalitis. The true frequency of this syndrome and its relationship to the frequent observation of transient polydipsia and polyuria in "benign" febrile illness remains to be determined.
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PMID:Transient diabetes insipidus with elevated serum osmolarity associated with 'benign' febrile illness. 92 28

In attempting to design an antagonist of the antidiuretic response to arginine-vasopressin (AVP) [1-deaminopenicillamine,4-valine,8-D-arginine]vasopressin (dPVDAVP) was synthesized by the solid-phase method and assayed for antidiuretic, vasopressor, and oxytocic activities. dPVDAVP has an antidiuretic potency of 123 +/- 22 units/mg, one-tenth that of its parent [deamino,4-valine,8-D-arginine]vasopressin (dVDAVP). Like dVDAVP its antidiuretic effect in conscious diabetes insipidus rats is greatly prolonged when compared to AVP. dPVDAVP causes a prolonged inhibition of vasopressor responses to AVP but not to norepinephrine or angiotensin II. It has an antivasopressor pA2 value of 7.82 +/- 0.05 when tested against AVP. Thus the penicillamine substitution at position 1 in dVDAVP increased its antivasopressor activity sixfold (dVDAVP has a pA2 value of 7.03 +/- 0.11). dPVDAVP is thus the most potent vasopressor antagonist yet reported. dPVDAVP was also found to be a potent inhibitor of the in vitro oxytocic response to oxytocin (pA2 value = 7.23 +/- 0.04). dPVDAVP with its potent and specific ability to antagonize the vasopressor effects of AVP should be a useful pharmacological tool with which to explore the possible participation of AVP's potent vasoconstrictor properties in cardiovascular regulation in physiological and pathological states.
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PMID:[1-deaminopenicillamine,4-valine]-8-D-arginine-vasopressin, a highly potent inhibitor of the vasopressor response to arginine-vasopressin. 92 26

Three children with diabetes insipidus, diabetes mellitus, optic atrophy, and high-tone deafness were shown to lack vasopressin, indicative of degeneration of the cells of the hypothalamic supraoptic nuclei. The syndrome being due to a single gene defect, inherited as an autosomal recessive, is therefore likely to be the result of an inborn error of metabolism with variable periods of latency in those affected.
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PMID:Diabetes insipidus, diabetes mellitus, optic atrophy, and deafness. 3 cases of 'DIDMOAD' syndrome. 93 28

Diabetes insipidus is an extremely rare condition complicating pregnancy. The deficiency in antidiuretic hormone production has led to the assumption that oxytocin synthesis may also be affected. For this reason spontaneous onset of labor in a number of previously reported cases has been considered as evidence against implicating oxytocin as a relevant factor in the evolution and maintenance of labor. For the first time, plasma oxytocin levels were determined in a patient with known idiopathic diabetes insipidus during pregnancy, labor, and postpartum, using radioimmunoassay. Oxytocin was not detectable in plasma before labor. There was however a surge of plasma oxytocin detected during labor and puerperium, a pattern somewhat similar to that seen in normal pregnancy. Our findings suggest that at least some patients with diabetes insipidus do secrete oxytocin and that the role of oxytocin, threfore, cannot be discounted in the labor process.
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PMID:Plasma oxytocin determinations in pregnancy with diabetes insipidus. 94 Jun 35

The acid phos phatase activity of the rat neurohypophysis was measured during increased gonadotrophic hormone levels, in diabetes insipidus (DI) (Brattleboro strain) and after water loading, i.e. conditions that interfere with the function of the hypothalamo-neurohypophyseal system (HNS). In addition determination of tissue protein, lipid and DNA and of water metabolism were performed. Neurohypophyseal acid phosphatase activity expressed on a dry weight basis increased under all conditions. For gonadectomized females, Brattleboro rats and water loaded males an increased water metabolism was observed. The increased acid phosphatase activity is interpreted as being related to disposal of release residues during stimulation of the HNS (increased gonadotrophic hormone levels and DI) and to disposal of neurosecretory material during inhibition (water loading).
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PMID:Acid phosphatase activity in the rat neurohypophysis during increased levels of gonadothrophic hormones, in diabetes insipidus (Bratteboro strain) and after water loading. 94 60

The etiology, diagnosis and management of lithium-induced diabetes insipidus (LIDI) is discussed, including the presentation of a case report. It is suggested that lithium provokes LIDI by decreasing the responsive ness of the kidney to the antidiuretic hormone. Lithium-induced polyuria may be managed by concomitant treatment with a thiazide diuretic or discontinuation of the lithium. Caution must be employed, however, when using thiazides with lithium as these diuretics decrease renal clearance of lithium.
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PMID:Lithium-induced nephrogenic diabetes insipidus. 94 67

A method was devised for the perfusion of the cerebral ventricles in conscious rats. Using this method a basal secretion rate of 15 +/- 3 pg of immunoreactive angiotensin II per min was calculated. This material was suggested to be of extrarenal origin. In comparison to findings in normal Long-Evans rats, pressor responses to intraventricular perfusions of angiotensin II were reduced in rats heterozygous for hypothalamic diabetes insipidus and virtually absent in rats homozygous for the hypothalamic deficiency whether they were treated with vasopressin or not. The pressor response to intraventricular angiotensin II is suggested to be related to the release of vasopressin.
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PMID:Pressor action of centrally perfused angiotensin II in rats with hereditary hypothalamic diabetes insipidus. 95 71

The symptomatic treatment of diabetes insipidus with pitressin is well known and very effective. The only problem concerns the type of pitressin to be used. In the past, pitressin snuff and various other intranasal instillations have been used, but these either have not been very effective, or have resulted in unpleasant side effects such as rhinitis. Until recently, the only effective form of the drug available in Australia has been pitressin tannate in oil. This often has to be given as a daily injection, which, like all intramuscular injections, is painful and, being in an oily base, is particularly likely to result in abscess formation. The recent introduction of 1-deamino-8-D-arginine-vasopressin (DDAVP), which can be simply instilled into the nostril, appears to present an advance in therapy.
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PMID:Diabetes insipidus treated by DDAVP. 95 68


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