Studies on the Mechanism of the Abnormal Sodium Excretion in Arterial Hypertension

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Abstract
Individuals with uncomplicated essential hypertension exhibit an abnormally high excretion of sodium and an associated impairment of urinary diluting and concentrating ability. Various possibilities have been considered to explain these related excretory changes including a solute diuresis resulting from diminished proximal tubular reabsorption of sodium, a reduction in sodium reabsorption from the ascending limb of the loop of Henle, and an increase in medullary blood flow. Evidence has been presented that does not support a defect in the sodium transport mechanism. On the other hand, the observed excretory abnormalities, when considered in terms of the reported pressure-dependent nature of the medullary circulation, could result from an increase in blood flow through the vasa recta secondary to the arterial hypertension.