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Significant hypertension was produced by DCA in intact, older rats given excess potassium, in contrast with the failure of hypertension to persist in similarly treated rats but receiving excess sodium. Potassium deficiency abolished the pressor action of DCA in rats. The results of these studies also indicated that the effects of DCA on the blood pressure were far more profoundly influenced by experimental variation of the potassium intake than that of sodium.
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Rosenman et al. (1951) studied this question.
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