A nomogram based on the relationship between plasma renin activity and urinary sodium excretion in normal subjects has been used to classify 956 patients with essential hypertension into low, medium and high renin subgroups. Patients with low renin hypertension (27 percent of all patients) were older (P less than 0.001) than patients with medium or normal renin hypertension. They also contained more women (P less than 0.01) and had higher systolic blood pressures than patients with medium renin hypertension. Creatinine clearance, albumin concentration and hematocrit were lower in low renin patients than in patients with medium renin activity. Serum potassium levels were lower, but urinary potassium excretion was higher in low renin patients. Most of the differences in clinical and biochemical parameters could be explained by the differences in age and male:female ratio between the subgroups. Despite lower renin values, aldosterone excretions were similar between the subgroups. Differences in renin activity and differences in aldosterone-renin ratio could not be explained by differences in age, duration of hypertension and sex ratios. Patients with low renin hypertension showed evidence of increased adrenal sensitivity to angiotensin II-induced aldosterone secretion. Patients with high renin hypertension (11 percent of all patients) were younger than patients with medium or normal renin hypertension. Other differences in biochemical characteristics between these renin subgroups included a slightly higher albumin concentration and hematocrit in patients with high renin levels. These differences and the difference in renin activity between patients with high and patients with medium renin essential hypertension could not be explained by differences in age and/or sex ratio between the two subgroups. Despite the higher renin activity, aldosterone excretion was similar between the high and medium renin subgroups. Therefore, patients in the high renin subgroup are characterized by signs of volume contraction and by a relative unresponsiveness of the adrenal gland to angiotensin II-induced aldosterone secretion. The possible role of these differences in the sensitivity of the adrenal gland in sustaining hypertension has yet to be defined.