The participation of the cellular sodium content and renin-angiotensin-aldosterone system in the development of high blood pressure has been frequently suggested. To elucidate the role of a mechanism responsible for renal sodium reabsorption on the time-course of renin suppression, 16 young borderline hypertensive patients were studied by analyzing the relationship between the level of baseline activation of lymphocyte Na+:H+ exchange and the degree of plasma renin activity (PRA) suppression in response to saline loading. In the whole hypertensive population, a significant correlation (R = 0.64; p < 0.01) was found between the lymphocyte Na+:H+ exchange activity and the percentage degree of PRA suppression induced by saline loading. Urinary sodium excretion was enhanced in patients with lesser activation of lymphocyte Na+:H+ exchange and greater PRA suppression (3.5 +/- 5 vs. 2.4 +/- .1 umol/min/kg; p < 0.05). These findings suggest that a mechanism influencing renal sodium reabsorption as Na+:H+ exchange could also affect the control of plasma renin activity, and concur with the development of salt-sensitive high blood pressure.