Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arginine8-vasopressin (AVP, 40 micrograms/100 g b.wt., SC) was administered to male Long-Evans (LE) pups from day 1 to 7 of life and the pups were sacrificed on day 8 or 60. 3H-AVP binding was performed on membranes prepared from the liver, kidney, and septum. No significant changes were observed in the kidney or septum of animals 8 or 60 days old. However, the chronic AVP treatment did result in a significant increase in the density of 3H-AVP binding sites in the liver when compared to control day 8 pups (control 44 +/- 2 vs. AVP 56 +/- 3 fmol/mg protein), with no change in affinity. This effect was maintained into adulthood, as the day 60 AVP-treated LE rats also showed a significant increase in liver 3H-AVP binding sites compared to control (control 186 +/- 9 vs. AVP 239 +/- 14 fmol/mg protein), with no change in affinity. A comparison of 3H-AVP binding sites in 8-day-old LE, heterozygous Brattleboro (HET-BB), and homozygous Brattleboro rats (HOM-BB) was performed to assess the effect of complete (HOM-BB) and partial (HET-BB) VP deficiency on binding sites in the CNS and periphery. The liver again was the only tissue in which a change in 3H-AVP binding characteristics was noted. The HOM-BB rat (Bmax 144 +/- 6 fmol/mg protein) displayed a significant increase in AVP binding sites from the LE rat (Bmax 100 +/- 7 fmol/mg protein), while the 3H-AVP binding sites in the HET-BB rat liver (Bmax 69.8 +/- 9 fmol/mg protein) were significantly lower than LE rats. Thus hepatic AVP receptors appear most sensitive to the presence or absence of vasopressin during the early postnatal period.
 ...
PMID:Effect of vasopressin administration and deficiency upon 3H-AVP binding sites in the CNS and periphery during development. 140 16

The role of vasopressin (VP) in a sexually dimorphic behavior, the extinction of a conditioned taste aversion, was investigated in male and female rats of three different genotypes. This behavior was examined with a two bottle test in the wild-type Long-Evans (LE) rats, and then in partially VP deficient heterozygous (HET-BB) and completely VP deficient homozygous (HO-BB) Brattleboro rats. In Experiment 1, non-deprived male and female LE rats were given aversions to a sucrose solution by pairing it with a LiCl injection. The rate of extinction of the aversion upon reexposure to ad lib sucrose solution was examined and observed to be sexually dimorphic. Female LE rats extinguished at a significantly more rapid rate than males. Experiment 2 compared HET-BB and HO-BB male and female rats using the same paradigm. Neither of these VP-deficient groups showed sexual dimorphism of the extinction behavior. The data suggest that intact VP levels are necessary to observe the expression of this sexually dimorphic behavior.
 ...
PMID:Vasopressin deficiency abolishes a sexually dimorphic behavior in Brattleboro rats. 159 83

The Brattleboro homozygous diabetes insipidus (HOM-DI) mutant rat, incapable of synthesizing the neuropeptide vasopressin, has an impaired body growth of which the severity depends upon the conditions of reproduction. The comparison of homogeneously genotyped litters of HOM-DI and heterozygous (HET-DI) control pups, delivered and nursed by HOM-DI females, was regarded to be the only experimental design that practically excludes other influences on growth differences than the mutation itself. In this breeding scheme the postnatal growth of the HOM-DI brain is impaired, and the weight deficit persists into adulthood. Regionally, the neonatal development of cerebellum and medulla oblongata is most affected, and only slightly that of the cerebral cortex. The other separately isolated parts of the the brain seem to be unaffected (olfactory bulbs, hypothalamus, hippocampus, colliculi and thalamus plus basal ganglia). Cerebellum appeared to be the most consistently affected brain area of the HOM-DI Brattleboro rat since, unlike in the case of cerebral cortex and medulla oblongata, the weight deficit persisted throughout life. Olfactory bulb growth, on the other hand, appeared to continue after the first month of life, resulting in an increased weight at day 180. Water content of cerebral cortex and cerebellum of HOM-DI adults appeared slightly higher and might be explained by the generation of different brain water regulation systems for HET- and HOM-DI Brattleboro rats. Protein and DNA estimations of cerebral cortex, cerebellum and olfactory bulbs of male brains during development and in adulthood reflect the differences as found for weight, indicating no obvious changes in cell densities. It is concluded after comparison with other types of brain growth malformations, that the HOM-DI Brattleboro brain has its own particular etiology. The possible involvement of the action of vasopressin is postulated and discussed.
 ...
PMID:Impaired brain development of the diabetes insipidus Brattleboro rat. 707 63

We examined whether a different maternal genotype might differentially affect the brain adrenocorticoid receptor in homozygous diabetes insipidus Brattleboro rats. Two distinct homozygous diabetic offsprings were studied in comparison with Long Evans (LE) rats: one born of a homozygous mother (DI/HOM MOTHER), and the other born of a heterozygous mother (DI/HET MOTHER). The number of type I adrenocorticoid receptors of DI/HET MOTHER rats was significantly lower than that of LE rats in the hippocampus and hypothalamus, while in the amygdala both type I and type II receptors decreased. Surprisingly, the binding capacity of DI/HOM MOTHER rats, notwithstanding the absence of vasopressin (VP), as in the DI/HET MOTHER, did not differ from that of LE. Superimposable results were obtained in all the brain regions examined. No differences in binding affinity values (Kd) were detected. It was hypothesized that an 'unknown factor' linked to the genotype of the homozygous diabetic mother might counterbalance the receptor deficit otherwise induced by the lack of VP. The existence of two subpopulations of diabetic Brattleboro rats, as used in this study, should prompt to reexamine the origins of some behavioral and endocrine discrepancies appearing in studies on the homozygous diabetes insipidus Brattleboro strain.
 ...
PMID:Brain adrenocorticoid receptor binding capacity in the diabetes insipidus brattleboro rat is dependent on maternal genotype. 839 18

In order to establish whether vasopressin (VP) influences brain cell survival, [3H]thymidine was injected in 10-day-old vasopressin-deficient Brattleboro rat pups, as well as in Wistar pups treated, neonatally, with the VP antagonist dP[Tyr(Me)2]VP followed by subsequent measurement of [3H]DNA in olfactory bulbs and cerebellum days and weeks thereafter. Results show, first of all, that the incorporation of [3H]thymidine into DNA was enhanced in the homozygous (HOM) Brattleboro, when compared with the heterozygous (HET; non-vasopressin-deficient) controls. The difference is due to the greater and prolonged tissue availability of [3H]thymidine, possibly pointing to an altered thymidine uptake and/or metabolism. Between postnatal days 25 and 39 no differences were seen in [3H]DNA content of the brain parts of the HET and Wistar control rats. For the HOM rats, however, a loss of [3H]DNA was seen (up to 8%), indicating that increased postnatal brain cell death might occur in the mutant. The antagonist treatment in Wistar rat up to 21 days of age failed to show a similar effect. It is proposed that general growth impairments, rather than VP receptor-mediated effects, lead to the brain cell loss.
 ...
PMID:Increased loss of brain DNA in the neonatal vasopressin-deficient Brattleboro rat, but not in normal rat treated with vasopressin antagonist. 841 82