Animal models for osmoregulatory disturbances.
For the various types of di in humans, animal models are available. However, their value for explaining human di is for the major part an indirect one; by studying cellular mechanisms in these animal models, fundamental aspects of the cellular processes become available, which will help to understand similar processes in human di and subsequently lead to the molecular cause(s) of the various types of human di. Finally, it is to be expected that in the very near future transgenic animals will be raised in which very specific genetic information is overexpressed (or knocked out by homologous recombination; McMahon and Bradley, 1990). Recently hypervasopressinemia could be shown in transgenic mice, providing an animal model for the syndrome of the inappropriate VP secretion (Bartter and Schwartz, 1967), which is often observed in patients with lung cancers that ectopically express the VP gene (Habener et al., 1989). Furthermore it will be possible to study the exact cause(s) of human di by performing in vitro mutagenesis and to express the RNA constructs within a cell-free translation system and in oocytes (e.g., Schmale et al., 1989) and subsequently study the pattern of precursor synthesis, packaging and processing.
Van Leeuwen
F W
FW
Netherlands Institute for Brain Research, Amsterdam.
D000595:Amino Acid Sequence; D000809:Angiotensins / Q000235:genetics*; D000818:Animals; D003919:Diabetes Insipidus / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D006801:Humans; D007031:Hypothalamus / Q000473:pathology / Q000503:physiopathology*; D051379:Mice; D008817:Mice, Mutant Strains; D008969:Molecular Sequence Data; D051381:Rats; D011910:Rats, Brattleboro; D014883:Water-Electrolyte Imbalance / Q000473:pathology / Q000503:physiopathology*
D000809:Angiotensins