EFFECTS OF CHRONIC EXCESS SALT INGESTION: EXPERIMENTAL HYPERTENSION IN THE RAT.
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Biomedical subjects
Publications and source records attributed to L K DAHL.
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By selective inbreeding, two strains of rats were developed previously that differed markedly in their susceptibility to the development of experimental hypertension from excess salt ingestion (1, 2). The present report indicates that with animals derived from the same strains, similar differences in response were obtained in rats subjected to either combined desoxycorticosterone-NaCl (DOCA-salt) treatment or unilateral renal artery compression without extra dietary salt. Thus differences in genetic substrate appear to influence the development of experimental hypertension produced by these three techniques and possibly this may hold true for all "varieties" of experimental hypertension. If true, it might allow the development of a unifying hypothesis that could be relevant not only to experimental hypertension but perhaps to human hypertension as well. The DOCA-salt regimen was more toxic to the animals than unilateral renal artery compression. Tentatively, this was ascribed to either, or both, the younger age or the higher NaCl intake of the animals in the former.
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Using the genetic technique of selective inbreeding, it has been possible to quickly develop two statistically separable populations from one unselected strain of Sprague-Dawley rats. One of these is very sensitive, the other very resistant, to the development of experimental hypertension from a high salt diet. It was suggested that similar genetic factors operate in man.
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Hypertension was induced in female rats by chronic feeding of sodium-containing salts in excess. The hypertension so induced appeared to be self-sustaining since about two-thirds of the animals failed to show a significant fall in blood pressure after withdrawal of these salts from the diet. Under the conditions of these experiments a lack of response to restriction of dietary sodium does not exclude an etiologic relationship between salt intake and development of hypertension.
Female rats were fed diets containing either excess sea salt or excess sodium chloride for periods up to 14 months. The hypertension produced by sea salt was more pronounced than that caused by sodium chloride alone, although the average amount of sodium chloride contained in the sea salt feeding was slightly less. The ions involved in this incremental effect of sea salt were not identified.
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