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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.
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