Pressor Effects of Epinephrine, Norepinephrine and Desoxycorticosterone Acetate (DCA) Weakened by Sodium Withdrawal

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Abstract
Recent findings suggest an important role of the sodium ion, intracellularly deposited by the adrenal mineralocorticoids, as the physicochemical mediator between the pressor actions of the mineralocorticoids and of the adrenosympathogenic neurohormones. The following observations show that the pressor effectiveness of both the pressor neurohormones and desoxycorticosterone acetate depends on the availability of sodium. This supports the theory that vascular pressor responsiveness and tonus is determined jointly by the sodium-depositing corticoids as sensitizers and the adrenosympathogenic neurohormones as the physiologic stimulators of the vascular contractile elements.