A 5-component mathematical model for salt-induced hypertension in Dahl-S and Dahl-R rats
There is considerable evidence which can be interpreted to indicate a familial trend in human essential hypertension (1-5). A familial disease could be due exclusively to common environmental factors, exclusively to common genetic patterns, or to an interaction of the two. For some years we have been exploring the effects of chronic excess salt ingestion in both man and animals and have brought forward evidence to support the thesis that dietary salt plays an etiologic role in human essential hypertension (6-12). However, it was observed repeatedly that some individuals, and some rats, remained normotensive despite the fact that they were chronically consuming large amounts of salt. In our nutritional experiments with rats (13-15) the control of environmental factors was rigid. In spite of this, in a given group, some salt-fed animals never developed hypertension whereas a few became hypertensive after 1 month on the diet and rapidly developed fulminating hypertension. I t was thought that such wide variations in response to excess salt consumption represented either the statistical limits of a homogeneous populatoin or the extreme consequences of genetic heterogeneity. If the population were homogeneous, it would not lend itself to fractionation by genetic techniques. By contrast, if sensitivity to salt were genetically controlled, it should be possible to separate two strains that differ demonstrably in the incidence and gravity of hypertension developing from excess salt consumption. The present paper is a report of experiments that resulted in the separation of two strains of rats differing markedly from one another in their susceptibility to the development of experimental hypertension from excess salt ingestion.