There is evidence that the usual variety of high blood pressure is, in part, a familial disease. Since families have similar genes as well as similar environments, familial diseases could be due to shared genetic influences, to shared environmental factors, or to both. For some years, the role of one

environment factor commonly shared by families, namely dietary salt (i.e., sodium chloride), has been studied at Brookhaven National Laboratory. These studies suggest that long excess salt intake 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 long successive generations of those animals that failed to develop hypertension from salt intake, 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, sensitive strain (the" S" strain) has also been developed.

The availability of these two strains permits investigations possible. They provide a plausible laboratory model on which to investigate some clinical aspects of the human hypertension. More important, there might be the possibility of developing methods by which genetic susceptibility (敏感性) 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.