Effects of Aldosterone on Blood Pressure and Electrolyte Distribution in the Rat

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Abstract
Aldosterone racemate, 20–40 µg, induced a small rise in blood pressure in the intact or nephrectomized rat following subcutaneous or intravenous but not intraperitoneal injection. It was effective in restoring the depressed pressure of the adrenalectomized animal towards normal within 60 minutes of intravenous administration. Extracellular fluid volume (inulin space) and extracellular Na were increased in the nephrectomized rat, but not in the nephrectomized-adrenalectomized animal during the restoration of blood pressure. Aldosterone racemate, 20 µg, also caused a characteristic increase in pressor sensitivity to Pitressin within 30 minutes of subcutaneous administration. Based on these findings and our previous studies, argument is presented to link the neurohypophysis and mineralocortex, both acting by different means in the same direction, with the control of sodium distribution between cells and environment. Vascular smooth muscle tonus is considered to be a function of the continuously regulated sodium gradient and thus of the sodium transfer systems. Plasma sodium changes in diverse states with altered blood pressure are considered to be evidence of attempts at compensation for an altered sodium gradient rather than as causal in themselves.