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Cited by 301

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Familial hypothalamic diabetes insipidus in rats (Brattleboro strain)

Valtin, H., Schroeder, H. A.·1964·American Journal of Physiology-Legacy Content

Abstract

Familial hypothalamic diabetes insipidus ( DI) has arisen as an apparently spontaneous mutation from a strain of Long-Evans hooded rats being bred for unrelated researches not involving radioactivity. The DI rats decrease water intake and urine flow, and increase urine osmolality in response to injected vasopressin. They concentrate their urines only minimally or not at all in response to dehydration, hypertonic saline, nicotine, or stress, and their serum osmolalities and sodium concentrations are significantly higher than those of normal animals. They show marked diminution of neurosecretory material in the neurohypophysis and supraoptic nucleus. The data suggest that the deficiency causing DI in these rats is a lack or dearth of synthesis of vasopressin or its carrier protein, or both.

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Metadata

Authors
Valtin, H., & Schroeder, H. A.
Venue
American Journal of Physiology-Legacy Content
Published
1964-02-01
Volume
206
Issue
2
Pages
425-430
ISSN
0002-9513 (ISSN-L)
OpenAlex
W2123319302
Cited by
301
References
0
FWCI
8.83
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Familial hypothalamic diabetes insipidus in rats (Brattleboro strain). https://app.cochat.ai/papers/10.1152/ajplegacy.1964.206.2.425
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Valtin, H., & Schroeder, H. A. (1964). Familial hypothalamic diabetes insipidus in rats (Brattleboro strain). American Journal of Physiology-Legacy Content. https://doi.org/10.1152/ajplegacy.1964.206.2.425

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.