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families havesimilar genes as well as similar environments, familial diseases could be due to shared genetic influences, to sharedenvironmental factors, or to both. For some years, the role of one environment factor commonly shared by familiesnamely dietary salt, has been studied at Brookhaven National Laboratory. These studies suggest that long excess saltintake can lead to high blood pressure in man and animals. Some individuals, however, and some rats consume largeamounts of salt without developing high blood pressure. No matter how strictly all environmental factors werecontrolled in these experiments, some salt-fed animals never developed hypertension(  ) whereas a few rapidlydeveloped 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, aresistant strain (the " R" strain) has been evolved in which consumption of large quantities of salt fails to influence theblood pressure sianificantly, in contrast, by mating only animals that auickly develop hypertension from salt. sensitivestrain (the "s" strain) has also been developed.
The availability of these two strains permits investigations possible. They provide a plausible (看 似合理的)raboratory model on which to investigate some clinical aspects of the human hypertension. More important, theremight be the possibility of developing methods by which genetic susceptibility (  ) of human beings to high bloodpressure can be defined without waiting for its appearance. Radioactive sodium (  ) 22 was an important "tool" inworking out the characteristics of the sodium chloride metabolism (氯 化钠代谢) .
The study of the effects of salt on high blood pressure was carried out .
Passage one
There is evidence that the usual variety of high blood pressure is, in part, a familial disease. Since