• 1 January 1975
    • journal article
    • research article
    • Vol. 33  (4) , 509-517
Abstract
Female rats of 2 Sprague-Dawley sub-strains and of the Wistar and Fischer 344 strains were sensitized to the hypertensogenic effect of excess salt by removal of 1 kidney and by being given 1% NaCl solution as their sole drinking fluid. One of the Sprague-Dawley sub-strains (SPD) and the Wistar (CFEP) rats developed progressive saline polydipsia of equivalent degree, blood pressure rose, and about 1/2 of the members became hypertensive during treatment. Rats of the other Sprague-Dawley strain (CFNP) also showed a progressive saline intake; but although they drank substantially less saline, the incidence of hypertension among them was increased by 50%. Animals of the Fischer 344 strain displayed neither saline polydipsia, the intake remaining relatively constant at a very low level throughout the experiment, nor hypertension. Salt hypertension appears to be affected by genetic factors in at least 2 ways, one of which regulates the quantity of salt ingested (salt appetite), while the other controls the susceptibility to salt excess or perhaps to hypertension per se. Fischer 344 rats have the ability to restrict the volume consumption of saline; their resistance to enforced high salt intakes has yet to be established.

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