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)

Modification of the natural vasopressin molecule to form desmopressin acetate (DDAVP) resulted in a compound with prolonged antidiuretic activity and virtual elimination of vasopressor activity. Twenty-one patients with central diabetes insipidus who ranged in age from 3 to 68 years were treated with DDAVP, which was administered intranasally in a dosage ranging from 10 microgram every 12 hours to 20 microgram every eight hours. Effective control of symptoms was obtained in all cases. There were no consequential toxic effects. As previously reported, DDAVP appears to be the preferred drug for the management of central diabetes insipidus. Biochemical alteration of hormones may enhance desired therapeutic activity and eliminate toxic effects. The development of DDAVP is an example of the potential for development of useful therapeutic peptides.
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PMID:Treatment of central diabetes insipidus in adults and children with desmopressin. 68 29

The effects of a synthetic analogue of vasopressin, DDAVP (1-deamino-8-D-arginine vasopressin) were investigated in 98 patients with cranial diabetes insipidus. In all patients, intranasal administration of DDAVP one to three times daily, usually twice daily, was found to be satisfactory in the control of diabetes insipidus. Thus, by DDAVP administration, daily urinary volume changed from 3520 +/- 2150 ml to 1620 +/- 830 ml (mean +/- SD), and urinary osmolarity changed from 126 +/- 75 mOsm/kgH2O to 446 +/- 194 mOsm/kgH2O (mean +/- SD). A daily dose of DDAVP ranged from 2.0 to 20 microgram in children (average dose 12.8 microgram), while 10 to 20 microgram of DDAVP was usually required in adult patients (average dose 14.2 microgram). No serious side effects have been observed. It is concluded that DDAVP is safe and effective in the treatment of cranial diabetes insipidus.
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PMID:[The treatment of patients with diabetes insipidus by a synthetic analogue of vasopressin, DDAVP (author's transl)]. 68 12

Desmopressin acetate is a synthetic vasopressin analogue administered by the intranasal route. It is long-acting and well tolerated and may be the agent of choice for treating central diabetes insipidus.
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PMID:Evaluation of a new antidiuretic agent, desmopressin acetate (DDAVP). 69 Dec 4

Studies demonstrating the antagonism by prostaglandins (PGs) of antidiuretic hormone (ADH) action led to the proposal that renal medullary PGs may act to attenuate the physiologic effects of ADH via a negative-feedback loop. Therefore, we examined urinary PG excretion, an indicator of renal PG synthesis, in rats with hereditary diabetes insipidus (DI) utilizing gas chromatography-mass spectrometry. The DI rats, devoid of ADH, excrete much less prostaglandin E2 (PGE2) than normal Long-Evans rats (39 +/- 5 vs. 228 +/- 53 ng/24 h, means +/- SE, P less than 0.005). DI and normal rats were treated for 35 days with ADH while separate groups of DI and normal controls received vehicle only. The ADH treatment increased urinary PGE2 excretion in DI rats to 233 +/- 35 ng/24 h whereas PGE2 excretion was unaffected by vehicle treatment. ADH treatment in normal rats similarly increased PGE2 excretion from 215 +/- 49 to 410 +/- 63 ng/24 h (P less than 0.05). To determine whether the rise in PGE2 excretion is the result of the rise in papillary osmolality, we subjected DI rats to dehydration, which increased urine osmolality from 130 +/- 10 to 302 +/- 12 mosmol/kg H2O but left urinary PGE2 unaffected. We conclude that ADH stimulates renal medullary PGE2 synthesis in vivo.
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PMID:Antidiuretic hormone increases renal prostaglandin synthesis in vivo. 69 28

Two patients with hypodipsia and hypernatremia are described. The first patient, whose hypodipsia was of unknown cause, developed hypernatremia unless large volumes of fluid were urged upon him; upon treatment with chlorpropamide normal serum sodium levels were achieved with spontaneous fluid intake. The second patient had hypodipsia and diabetes insipidus resulting from a craniopharyngioma. Treatment with vasopressin and a prescribed daily water intake resulted in frequent hyper- and hyponatremia, but treatment with chlorpropramide yielded serum sodium values which were more often normal and less variable. In neither patient could the improved water regulation be attributed to an effect of chlorpropamide on renal water excretion. Possible mechanisms for the effect of chlorpropamide on thirst are discussed.
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PMID:Successful treatment of hypernatremic thirst deficiency with chlorpropamide. 69 8

A follow-up study was carried out on 12 children with vasopressin sensitive diabetes insipidus. 1) Nine cases (75%) of 12 were finally diagnosed as having brain tumor in later course. There were 3 cases (25%) who could not be decided as having brain tumor during the follow-up period of more than 6 years. 2) There was one case who developed the overt signs of brain tumor 9 years after the onset of diabetes insipidus. Therefore, it seems necessary to follow-up cases with diabetes insipidus for at least 10 years before determining it as idiopathic type. 3) In cases with diabetes insipidus due to brain tumor, associated growth retardation, autonomic symptoms, behavior disorder, endocrine dysfunction and metabolic dysfunction were frequently observed. In the case where these symptoms become aggravated with lapse of time, these findings should be taken seriously as indicating brain tumor. 4) In the case showing either anterior or posterior focal slow waves in the EEG, if such focal slow waves aggravate with age, the findings should be considered as indicative of brain tumor. 5) We would like to emphasize the significance of brain tumor as the underlying pathology of childhood diabetes insipidus.
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PMID:[Diabetes insipidus in children--long-term follow-up study]. 70 11

We have described a 13-year-old white boy with Ondine's curse, sleep apnea and cataplexy who simultaneously developed progressive hypothalamic neuroendocrine deficiencies requiring replacement therapy. The patient was treated with protriptyline, a nonsedating tricyclic antidepressant, for control of the sleep-related symptoms. An unexpected result was the apparent reversal of his chronic diabetes insipidus by protriptyline, necessitating discontinuation of lysine-vasopressin. Some possible mechanisms of action were discussed.
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PMID:Reversal of chronic diabetes insipidus during treatment with protriptyline. 72 36

On the assumption that the antagonism between prostaglandin E2 and vasopressin might represent a negative feedback system, we evaluated the hypothesis that vasopressin stimulates, in vivo, the renal production of prostaglandins. For these studies we used Brattleboro homozygous rats with diabetes insipidus and Long-Evans rats for controls, Brattleboro homozygotes show a substantial reduction in the renal excretion of prostaglandin E2 and prostaglandin F2alpha. Homozygotes excreted 39 +/- 5 ng/24 h prostaglandin E2 and 40 +/- 4 ng/24 h prostaglandin F2alpha, compared to 217 +/- 40 and 221 +/- 18 ng/24 h, respectively, in control rats (P less than 0.001). Therapy of homozygotes with vasopressin tannate in oil resulted in a prompt increase in the urinary excretion of prostaglandin E2 and prostaglandin F2alpha. 1-Desamino-D-arginine vasopressin, a nonpressor analogue of vasopressin, also enhanced the renal production of prostaglandin E2. We conclude that vasopressin (antidiuretic hormone) stimulates renal production and excretion of prostaglandin E2 and prostaglandin F2alpha in vivo. It is possible that this increment of prostaglandin synthesis serves a negative feedback function by modulating the action of vasopressin on the renal tubule.
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PMID:Renal excretion of prostaglandins E2 and F2alpha in diabetes insipidus rats. 73 21

The water metabolism was studied in homo- and heterozygous Brattleboro rats suffering from hereditary hypothalamic diabetes insipidus. In homozygous Brattleboro rats the spontaneous water intake and urinary output and the diuretic reactions signficantly increased after water and salt loading. No antidiuretic activity was found in the urine, posterior pituitary or hypothalamus of these animals, and this state was not affected by hyperosmosis. For the heterozygous rats the spontaneous water intake and urinary output and the diuretic reaction exceed the respective control values, the posterior pituitary, the hypothalamus and the urine are of reduced antidiuretic activity and this activity is less mobilizable by hyperosmosis. It is concluded that the ADH-reserve deficiency is total in the homozygous Brattleboro rats, and partial in the heterozygotes. As a result of hyperosmosis, the vasopressin release is of a reduced extent, yet detectable in the heterozygotes.
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PMID:The ADH-reserve capacity in Brattleboro rats. 74 41

A synthetic vasopressin analog, 1-desamino-8D-arginine vasopressin (DDAVP also known as desmopressin), was found to be highly effective in the treatment of seven children and one adult with vasopressin-sensitive diabetes insipidus. The average duration of action of DDAVP was 10 to 11 hours, and with proper adjustment of dose, the subjects were able to control their symptoms satisfactorily with one or two inhalations daily. The youngest child in whom adequate control was achieved was 2 years of age. All subjects found the use of intranasal DDAVP superior to other forms of therapy, and none experienced any known side-effects after six months of treatment. All subjects in this study are currently using 2.5 mug to 10 mug of DDAVP once or twice daily.
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PMID:Vasopressin analog DDAVP in the treatment of diabetes insipidus. 76 13


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