Disease relevance of Rats, Brattleboro

• Single base deletion in the vasopressin gene is the cause of diabetes insipidus in Brattleboro rats [1].
• Vasopressin neurons, transplanted from normal rat fetuses into the third ventricle of adult Brattleboro rats, alleviate the polydipsia and polyuria of the hosts [2].
• The roles of vasopressin and calcineurin in PAN nephrosis were evaluated by measuring these parameters in Brattleboro rats and in rats treated with cyclosporin or tacrolimus [3].
• Finally, the lack of vasopressin in Brattleboro rats or the inhibition of calcineurin by administration of either cyclosporin or tacrolimus did not prevent development of the nephrotic syndrome in PAN-treated rats or stimulation of CCD (Na+/K+)-ATPase [3].
• Persistent phenotypic correction of central diabetes insipidus using adeno-associated virus vector expressing arginine-vasopressin in Brattleboro rats [4].

Psychiatry related information on Rats, Brattleboro

• Further, in homozygous Brattleboro rats, in which endogenous vasopressin is absent, food deprivation caused changes in urine volume, urine osmolality, and AQP2 expression, which are qualitatively similar to those observed in normal rats [5].
• Binding sites for rat atrial natriuretic peptide (6-33) (ANP) were quantitated in the subfornical organ of chronically dehydrated homozygous Brattleboro rats unable to synthesize vasopressin; heterozygous Brattleboro rats, their controls, Long Evans rats and Long Evans rats after 4 days of water deprivation [6].
• Circadian rhythms in wheel running and drinking behavior were investigated using heterozygous an homozygous (diabetes insipidus) female Brattleboro rats Despite the lack of vasopressin in the suprachiasmatic nuclei of the diabetic rats, they showed coherent rhythms, both in cyclic light and in constant light [7].

High impact information on Rats, Brattleboro

• This defect has been presumed to be at the genomic or transcriptional level, as AVP messenger is reported to be drastically reduced, if not absent, from the hypothalamus of Brattleboro rats [8].
• Homozygous (di/di) Brattleboro rats have normal hypothalamic levels of oxytocin and neurophysin I, but undetectable levels of neurophysin II and arginine-vasopressin (AVP) [8].
• In vivo, AVP is able to stimulate ACTH secretion, and Brattleboro rats, deficient in AVP, show a reduced activity of the hypothalamo-hypophysial-adrenocortical system (HHCS) (see ref. 13 for references) [9].
• Homozygous Brattleboro rats (deficient in vasopressin) have magnocellular neurons that contain dynorphin separate from oxytocin [10].
• The activity of angiotensin-converting enzyme is significantly higher in the intermediate and posterior pituitary lobes of Brattleboro rats than in Long-Evans control rats [11].

Chemical compound and disease context of Rats, Brattleboro

• [3H]GEMSA labeling in the intermediate pituitary lobe is unaffected by dehydration and haloperidol treatment and in Brattleboro rats [12].
• 1. In previous experiments in conscious, water-replete Long Evans and Brattleboro rats the non-peptide angiotensin II-receptor antagonist, DuP 753, caused only slight hypotension and peripheral (particularly renal) vasodilatations [13].
• Exogenous corticosterone acetate attenuates the hypotension induced by ganglion blockade in conscious Long Evans and Brattleboro rats [14].
• 1. The cardiovascular effects of bolus intravenous injections of vasopressin, angiotensin II and noradrenaline were studied in 6-hydroxydopamine pretreated, anaesthetized Brattleboro rats with hereditary diabetes insipidus and normal rats of the parent Long Evans strain [15].
• These tubular epithelial lesions were not seen in the kidneys of Brattleboro rats or glucose-treated Wistar rats despite comparable polyuria [16].

Biological context of Rats, Brattleboro

• These results indicate that AVP-replaced homozygous Brattleboro rats can regulate AVP gene expression normally in response to fluid deprivation [17].
• Heart rate fell in a dose-dependent manner after intracisternal AVP in Long Evans rats but not in Brattleboro rats [18].
• Long-term treatment of Brattleboro rats with a vasopressin analog markedly decreased adenylyl cyclase type 3 protein abundance, providing an explanation for long-term down-regulation of vasopressin response in the collecting duct [19].
• Vasopressin significantly increased UT-A1 phosphorylation in vasopressin-treated diabetic Brattleboro rats but not in the other groups of Brattleboro rats [20].
• Increased atrial natriuretic peptide (6-33) binding sites in the subfornical organ of water deprived and Brattleboro rats [6].

Anatomical context of Rats, Brattleboro

• Suprachiasmatic nucleus vasopressin messenger RNA: circadian variation in normal and Brattleboro rats [21].
• About 50% of supraoptic neurons in Long-Evans rats and 90% in Brattleboro rats were cNOS immunopositive; a qualitatively similar difference occurred in the paraventricular nucleus [22].
• Immunofluorescence labeling with the COOH-terminal antibody in Brattleboro rats revealed labeling in the lower portion of descending limbs from short-looped nephrons (in the aquaporin-1-negative portion of this segment) [23].
• The supernatant of homogenized 0.1 N acetic acid-extracted testis from adult homozygous Brattleboro rats was chromatographed on a Sephadex G-25 column [24].
• Incubation with vasopressin for 30 min increased the conversion of oleate into triacylglycerol by 17% and 32% in hepatocytes from Wistar and Brattleboro rats respectively [25].

Associations of Rats, Brattleboro with chemical compounds

• Homozygous Brattleboro rats (di/di) were fed a regular diet (0.5% histidine) or a diet enriched with histidine and received 1 ng of 1-deamino-8-D-arginine vasopressin (dDAVP) daily [26].
• Brattleboro rats had decreased binding of [3H]corticosterone per neuron, whereas aged subjects, in addition, had significant losses in the number of corticosterone-concentrating neurons [27].
• Indeed, Brattleboro rats, which lack endogenous AVP, with clamped blood dDAVP levels, showed no difference in dDAVP-generated cAMP generation between kidneys of rats with lithium-induced NDI and control rats [28].
• Renal tubular and vascular urea transporters: influence of antidiuretic hormone on messenger RNA expression in Brattleboro rats [29].
• Administering vasopressin (1 U/day) to Brattleboro rats for 8 days also increased urine osmolality and aldose reductase mRNA but did not alter sorbitol dehydrogenase or taurine cotransporter mRNA [30].

Gene context of Rats, Brattleboro

• Treating Brattleboro rats with desamino-Cys-1,d-Arg-8 vasopressin, which increases inner-medullary NaCl concentration, causes a 4-fold increase in inner-medullary Pax2 protein [31].
• Finally, the very low nNOS expression levels observed in AVP-deficient Brattleboro rats was restored by AVP infusion for 1 wk [32].
• Additionally, regions of CNT lacking AQP2 labeling could be identified in Brattleboro rats not treated with vasopressin but not in such animals chronically treated with deamino-Cys(1),D-Arg(8)-vasopressin (dDAVP) [33].
• Medullary COX-1 expression was moderately lower and COX-2 expression was significantly lower in adult male Brattleboro rats than age-matched Long-Evans controls [34].
• In protocol 3, Na restriction (to increase endogenous aldosterone levels) or exogenous aldosterone infusion in either normal rats or vasopressin-deficient Brattleboro rats was associated with a major increase in AQP3 abundance [35].

Analytical, diagnostic and therapeutic context of Rats, Brattleboro

• Immunoblotting and immunohistochemistry demonstrated that collecting ducts of vehicle-infused Brattleboro rats had markedly reduced expression of AQP-CD relative to normal rats [36].
• 1. Intake and output of water, Na+ and K+ were measured in Long Evans and Brattleboro rats (deficient in hypothalamic and pituitary vasopressin) before and after subcutaneous injection of polyethylene glycol (PEG) sufficient to cause a substantial hypovolaemia [37].
• This decrease is abolished by arginine vasopressin treatment of Brattleboro rats or rehydration of dehydrated rats [12].
• The purpose of the present experiments was to examine the expression of SLC26A7 in kidneys of vasopressin-deficient Brattleboro rats before and after treatment with desamino-Cys(1),d-Arg(8)-vasopressin (dDAVP) [38].
• Similar stimulation of papillary COX-2 resulted from DOCA treatment of normal control rats, but the response was blunted in rats fed a low-salt diet and absent in Brattleboro rats [39].

References