There is evidence that the usual variety of high blood pressure is, in part, a family disease. Since families have similar genes as well as similar environment, family diseases could be due to shared genetic influences, to shared environmental factors, or to both. For some years, the role of one's environmental factor commonly shared by families, namely, dietary salt, has been studied at Brookhaven National Laboratory. These studies suggest that chronic 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 develop 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 in 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 two strains permits investigations not heretofore possible. They provide a plausible laboratory model on which to investigate some clinical aspects of the human proto - types 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. Which statement relates the main idea of this passage?