ABSTRACT
Animal models are major tools for exploring complex physiological and pathological
processes offering experimental approaches that are inapplicable in humans and providing
the opportunity to perform studies in which all factors are kept constant, except those that
are evaluated (1). This latter possibility is critical for analyzing processes that arise from
the combined action of many genetic and environmental factors, each typically exerting
small effects on the overall processes (2). In practice however, investigators do not always
take full advantage of this opportunity. For example, the phenotype resulting from
a specific mutation is frequently different from one study to another due to the lack of
control of the genetic background (3-5). A large phenotypic variability can also arise from
the environment of the animals that can widely differ from one laboratory to another with
respect to the microbiological, viral and parasitic status of the breeding facility, the
physical housing conditions (temperature, humidity, light/dark cycle) and/or the diet.
Despite these inconsistencies, the investigations conducted in animal models during the
last decades have provided valuable insights concerning the mechanisms by which the
kidneys match urinary sodium excretion to dietary intake and the pathological phenotypes
linked to an abnormal renal sodium handling. This chapter briefly describes the large body
of data, which has been mostly gained in rodents, on the relationships between altered
renal capacity to excrete sodium and long-term control of blood pressure (6,7).
