Sodium metabolism in essential hypertension. Natriuretic response to acute hypertonic saline load.

In order to investigate the mechanism of the "exaggerated natriuresis" in hypertension, 300 ml of 3% saline was infused for 1 hour during hydropenia in 13 patients with normal renin essential hypertension and 5 normotensive subjects on a daily ingestion of 4 Gm and 16 Gm of NaCl. At the end of the infusion, the circulating blood volume indicated by the change in serum total protein concentration and the glomerular filtered load were increased in a similar manner in both groups. Prompt the enhanced natriuresis and diuresis were seen within 1--2 hours after starting the infusion in the hypertensives on a daily ingestion of 16 Gm of NaCl. Significant positive correlations were found between the change in mean arterial blood pressure (deltaMAP) and UV, and between deltaMAP and UNa V in the hypertensives either on a daily 4 Gm or 16 Gm ingestion of NaCl. Free water reabsorption (Tc H2O) was lower in the hypertensives than that in the controls at high levels of osmolar clearance (Cosm). Plasma renin activity (PRA) did not differ in either group on either NaCl ingestion and was equally suppressed on a daily ingestion of 4 Gm of NaCl, while little changed on a high salt intake. Plasma aldosterone levels changed in parallel with PRA. It is suggested that the "exaggerated natriuresis" is due to the decreased tubular sodium reabsorption, which may be the result of intrarenal hemodynamic changes related to the elevated renal perfusion pressure. The decreased medullary osmolar gradient probably induced by an increase in the medullary blood flow is a possible contributing factor in the enhanced sodium and water excretion, and the renin-aldosterone system does not seem to play an important role.