DETAILED STUDIES, in the preceding communication (p 213), on three subsequently proved cases of primary aldosteronism indicate conclusively that in the presence of an aldosterone-secreting tumor, plasma renin activity is suppressed to zero, and it cannot be increased above zero even after many days of severe sodium deprivation. Using the same method of extraction and assay for renin activity, a normal range was established from 18 healthy subjects studied under various conditions. In all cases renin activity of various intensities was easily measurable, and the values tripled upon restriction of sodium for 72 hours.2 The suppression of renal release of renin in primary aldosteronism is not due to a high blood level of aldosterone, per se, but rather to the increase in intravascular volume and pressure which is known to be associated with it.3,4The increase in "stretch"5at the baroreceptor site (juxtaglomerular cells) in the afferent