There is evidence that the usual variety of high blood pressure is, in part, a familiar disease. Since families have similar genes as well as similar environments, familiar diseases could be due to shared genetic influences, to shared environmental factors, or to both. For some years, the role of one environmental factor commonly shared by families, namely dietary salt (i.e., sodium chloride), has been studied at Brookhaven National Laboratory. These studies suggest that chromic excess salt ingestion can lead to high blood pressure in man and animals. Some individuals, however, and some rats consume large amounts of salt without developing high blood pressure. No matter how strictly all environmental factors were controlled in these experiments, some salt-fed animals never developed hypertension whereas a few rapidly developed very severe hypertension followed by early death. These marked variations were interpreted to result from differences in genetic constitution.
By mating is successive generations only those animals that failed to develop hypertension from salt ingestion, a resistant strain (the "R" Strain) has been evolved in which consumption of large quantities of salt fails to influence the blood pressure significantly. In contrast, by mating only animals that quickly develop hypertension from salt, a sensitive strain ("S" strain) has also been developed.
The availability of these tow strains permits investigations not heretofore possible. They provide a plausible laboratory model on which to investigate some clinical aspects of the human prototypes of hypertension. More important, there might be the possibility of developing methods by which genetic susceptibility of human beings to high blood pressure can be defined without waiting for its appearance. Radioactive sodium 22 was an important "tool" in working out the characteristics of the sodium chloride metabolism.