There are now three strains of hypertension-prone rats in which genetic factors are demonstrably involved in setting average blood pressure levels. The first strain was described by Smirk and Hall in 1958 (1), the second by Dahl et al. in 1962 (2, 3), and the third by Okamoto and Aoki in 1963 (4). Formal genetic studies indicated that blood pressure control was multigenic in all three strains (5-7). It is likely that these strains share some genes that control blood pressure but the available evidence is not consistent with the possibility that they share them all. Among a number of differences in these strains that suggest nonidentity of the gene pools controlling blood pressure, none is more evident than the response to excess dietary salt (NaC1). Both the New Zealand strain isolated by Smirk and Hall (1) and the spontaneously hypertensive rat (SHR) 1 separated by Okamoto and Aoki (4) develop significant hypertension without additional dietary salt, whereas the sensitive strain developed by Dahl et al. (2, 3) was originally evolved specifically on the basis of its hypertensive response to NaC1. The fact that some rats develop hypertension spontaneously on normal salt intakes led to the widespread belief that salt intake was therefore unimportant. In the aggregate, our long experience studying both clinical and experimental hypertension by modifying dietary NaC1 is incompatible with such a concept. The belief that dietary NaC1 is unimportant if elevations in blood pressure are insignificantly affected by increments or decrements in salt consumption represents, in our opinion, a simplistic view of such a lethal disease as hypertension. If there is evidence of increased mortality in association with increased salt intake or decreased mortality with decreased salt intake, whatever the effects on blood pressure, this is of consequence: the importance of survival in considerations affecting one of the major cardiovascular diseases is not to be underrated.The present work was done as part of a continuing long-term study in which the relative importance of dietary NaC1 and genetic makeup are being evaluated, in a variety of situations, in both clinical and experimental hypertension.