Sodium Metabolism in Essential Hypertension Natriuretic Response to Acute Hypertonic Saline Load

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Abstract
To study the mechanism of exaggerated natriuresis in hypertension, 300 ml of 3% saline was infused for 1 h during hydropenia in 13 patients with normal renin essential hypertension and 5 normotensive subjects on a daily ingestion of 4 g and 16 g NaCl. At the end of the infusion, the circulating blood volume indicated by the change in serum total protein concentration and glomerular filtration rate were increased to a similar extent in both groups. Prompt and enhanced natriuresis and diuresis occurred within 1-2 h after starting the infusion in hypertensives on a daily ingestion of 16 g NaCl. Significant positive correlations occurred between the change in mean arterial blood pressure (.DELTA.MAP) and UV [urine volume], and between .DELTA.MAP and UNaV [urine Na concentration] in the hypertensives either on a daily 4 g or 16 g ingestion of NaCl. Free H2O reabsorption (TcH2O) was lower in the hypertensives than 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 g NaCl, while little changed on a high salt intake. Plasma aldosterone levels changed simultaneously with PRA. Exaggerated natriuresis is possibly due to decreased tubular Na reabsorption which may be the result of intrarenal hemodynamic changes related to the elevated renal perfusion pressure. Decreased renal medullary osmolar gradient probably induced by an increase in the medullary blood flow is a possible contributing factor in the enhanced Na and H2O excretion and the renin-aldosterone system does not seem to be important.