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)

Administration of DDAVP (1 desamino-8-D-arginine vasopressin), a form of vasopressin with little pressor action, has been shown to improve cognitive performance in the elderly. It remains unclear whether memory processes are specifically influenced or more general processes are altered. Fifteen elderly subjects performed a central mental arithmetic task and a peripheral choice reaction time task in DDAVP and control conditions. DDAVP slowed reaction times to peripheral lights but did not alter arithmetic performance. The results suggest that DDAVP increases the proportion of attention allocated to primary task performance by decreasing attention to secondary tasks. This shift does not appear to be mediated by any action of DDAVP on peripheral cardiovascular function.
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PMID:Vasopressin peptide (DDAVP) may narrow the focus of attention in normal elderly. 394 98

The possibility that sympathetic nervous system activity may be altered in Brattleboro rats with diabetes insipidus (DI) was studied using the norepinephrine (NE) turnover technique. Female DI and Long-Evans rats were used. NE turnover in peripheral organs was calculated by measuring the decline in tissue [NE] after inhibition of tyrosine hydroxylase with alpha-methyltyrosine. NE turnover was increased significantly in the kidney of DI rats but was not significantly altered in other peripheral organs examined (heart, duodenum, skeletal muscle). Both NE and epinephrine concentrations in the adrenal gland were significantly higher in the DI rats. Treatment of DI rats for 7 days with vasopressin tannate (Pitressin, 100 mU/100 g) or 1-deamino-[8-D-arginine] vasopressin (DDAVP, 250 ng X kg-1 X day-1) reversed the changes in renal NE turnover and also decreased the turnover in other tissues. The results of these studies suggest that, compared with Long-Evans rats, DI rats have a selective increase in NE turnover in the kidney and the potential to release more catecholamines from the adrenal glands. The apparently nonspecific effect of antidiuretic therapy on NE turnover in DI rats is probably mediated by the epithelial receptor for vasopressin, because both Pitressin and DDAVP produced similar results.
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PMID:Enhanced noradrenergic activity in kidney of Brattleboro rats with diabetes insipidus. 396 26

The effect of chronic and acute treatment with DDAVP, a vasopressin analog, was studied in 2 month old male rats, using an active avoidance test in a shuttle box. The experiment lasted 6 weeks: an acquisition period of 4 weeks and an extinction period of 2 weeks. Rats were treated one hour before behavioral testing 3 times a week for 6 weeks with either DDAVP 20 micrograms/rat/day for the whole period (chronic group) or with DDAVP for the first week and again once only on the first day of the extinction period (acute group) or with saline. Chronic treatment with DDAVP resulted in better acquisition and in a marked retardation of extinction compared with the acute treatment group. These results were obtained both in normal rats and in rats pretreated at age 5 days of life with intracisternal 6-OH dopamine.
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PMID:The effect of chronic vs. acute injection of vasopressin on animal learning and memory. 399 61

To define how renal papillary epithelial cells respond to wide changes in the ionic and osmotic composition of their environment, measurements were made of the transmembrane potential differences (PD) of rat renal papillary epithelial cells in vitro in media containing 100 mM NaCl, 100 mM KCl, 1.5 mM CaCl2, and 1 mM MgSO4 plus varying amounts of urea and/or sucrose up to 1,400 mM. Glass microelectrodes (resistance 25-75 M Omega) were used. With added sucrose, no change in PD from the initial value of -9.3 +/- 1.3 (SD) mV (n = 29) (cell interior negative) was found. With added urea, alone or while osmolality was maintained nearly constant with sucrose, the PD changed in a triphasic manner, depolarizing to -5.3 mV at 50 mM urea, hyperpolarizing to -20.0 mV at 150 mM urea, and then depolarizing again to -5.5 mV at 1,400 mM urea. When bath potassium was decreased to 10 meQ/liter (choline replacement) the PD hyperpolarized to -46.9 +/- 5.0 (SD) mV (n = 32). DDAVP, a nonpressor vasopressin analogue, and 8-bromo-cAMP depolarized the membrane to -5 mV in the presence of urea but did not change PD when urea was absent. These observations suggest an interaction between urea and ionic movement or conductance in rat renal papillary epithelial cells.
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PMID:Transmembrane potential of renal papillary epithelial cells: effect of urea and DDAVP. 400 53

A case of delayed onset of diabetes insipidus (DI), which developed 27 days after a closed head injury, is reported. The patient sustained only a minor neurological deficit and, except for antidiuretic hormone (ADH) insufficiency, hypothalamic function was intact. This selective damage of posterior pituitary function was total and permanent. Ischemia due to vascular injury may be the most likely etiology. Once the diagnosis of delayed posttraumatic DI is confirmed, the treatment of choice is DDAVP (desmopressin acetate). In contradistinction to DI immediately following minor head injury, most patients with a delayed onset of DI after trauma have permanent ADH deficiency.
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PMID:Unusual delayed onset of diabetes insipidus following closed head trauma. Case report. 402 Apr 75

DDAVP has been shown to facilitate memory, especially retrieval, in humans. Healthy young male adult subjects received DDAVP (60 micrograms) in a cross-over design with a one-week interval between sessions. Results indicated that DDAVP improved immediate memory during the first but not the second testing session, particularly for low-verbal subjects. Treatment with DDAVP also facilitated delayed (one-week) recall in the opposite group, a cross-over interaction that suggests a retrieval locus for the DDAVP effect. Furthermore, since DDAVP improved immediate memory more for low-verbal subjects and delayed memory more for high-verbal subjects, it appears that individual difference factors will be important in understanding the effects of vasopressin on memory.
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PMID:Sentence memory affected by vasopressin analog (DDAVP) in cross-over experiment. 407 14

In seven patients with cranial diabetes insipidus an analogue of vasopressin, DDAVP, produced an antidiuresis lasting up to 20 hours after a single intranasal dose. Lysine vasopressin (LVP) in the same dose produced a less potent antidiuresis which lasted for only three to four hours. The plasma half life of DDAVP was 7.8 and 75.5 min for the fast and slow phases, compared with 2.5 and 14.5 min for LVP. Radioiodine-labelled DDAVP was not destroyed by incubation with late pregnancy plasma, which contains an enzyme that inactivates vasopressin. The slow metabolic clearance of DDAVP, its absorption through the nasal mucosa, and its lack of side effects make this the ideal drug for the treatment of vasopressin-sensitive diabetes insipidus. Patients usually require 10 to 20 mug DDAVP given intranasally twice daily for good clinical control of their diabetes insipidus.
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PMID:Vasopressin analogue DDAVP in diabetes insipidus: clinical and laboratory studies. 458 Oct 79

Vasopressin is reported to enhance learning and memory in animal models. In 9 Down's syndrome patients DDAVP, a vasopressin derivative, was administered for 10 days, 40 micrograms per day, in a double-blind randomized crossover design. A visual-verbal paired associate learning test showed a not significant tendency for benefit with DDAVP. Word List memory was not improved with DDAVP treatment.
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PMID:The effect of vasopressin treatment on learning in Down's syndrome. 623 33

In an attempt to clarify the mechanism responsible for the prolonged effect of DDAVP (1-desamino-8-D-arginine vasopressin), plasma levels of DDAVP and nephrogenous cyclic AMP were determined in patients with diabetes insipidus after a single intranasal administration of 10 micrograms of DDAVP. Plasma DDAVP levels were uniformly elevated within 30 min, and showed a peak ranging from 5.6 to 25.0 pg/ml between 30 and 120 min. The subsequent time-course of plasma DDAVP differed however, from patient to patient, and was irregular in most of them. In all of the patients whose plasma DDAVP dropped below 1.0 pg/ml, antidiuresis was still observed. Although the mean basal level of nephrogenous cyclic AMP in patients with diabetes insipidus was not significantly different from that in control subjects, the administration of DDAVP resulted in a 2-fold increase. A negative correlation between nephrogenous cyclic AMP and free water clearance was obtained. These results suggest that the long-acting nature of DDAVP may be attributed, in addition to its gradual absorption from nasal mucosa and slow metabolic clearance, to a higher or persistent biological activity at the receptor site in the kidney and that a nearly physiological level of antidiuretic hormone may cause de novo synthesis of cyclic AMP in the kidney and exert its biological action.
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PMID:Prolonged antidiuresis by 1-desamino-8-D-arginine vasopressin (DDAVP): correlation to its plasma levels and nephrogenous cyclic AMP production. 625 52

The role of vasopressin as a pressor agent to the hypertensive process was examined. Vasopressin plays a major role in the pathogenesis of DOCA-salt hypertension, since the elevation of blood pressure was not substantial in the rats with lithium-treated diabetes insipidus after DOCA-salt treatment. Administration of DDAVP which has antidiuretic action but minimal vasopressor effect failed to increase blood pressure to the levels observed after administration of AVP. Furthermore, the pressor action of vasopressin appears to be important in the development of this model of hypertension, since the enhanced pressor responsiveness to the hormone was observed in the initial stage of hypertension. Increased secretion of vasopressin from neurohypophysis also promotes the function of the hormone as a pathogenetic factor in hypertension. An unproportional release of vasopressin compared to plasma osmolality may be induced by the absence of an adjusting control of angiotensin II forming and receptor binding capacity for sodium balance in the brain. However, the role of vasopressin remains to be determined in human essential hypertension.
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PMID:Vasopressin as a possible contributor to hypertension. 632 16


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