The nonmodulating trait thought to explain development of hypertension
in 25 to 35% of patients, is characterized by abnormal angiotensin II
(AII)-mediated control of aldosterone release and renal blood flow (R
BF). Some data support the possibility that nonmodulation is an inheri
ted trait, but others argue that it is an acquired epiphenomenon of th
e hypertensive state. We report the first case of a normotensive patie
nt with nonmodulation who subsequently developed frank hypertension. P
atient RR was studied on six occasions over a 5-year period, two while
normotensive, four while hypertensive. This patient consistently demo
nstrated an abnormally low plasma aldosterone response to AII (3 ng/kg
/min) on a low salt (10 mEq sodium) diet while both normotensive and h
ypertensive. A consistently abnormally depressed RBF response to AII o
n a high salt (150 to 200 mEq sodium) diet as well as a depressed RBF
increment when the diet was changed from low salt to high salt were al
so noted. Thus, RR demonstrated nonmodulation by multiple criteria whi
le both normotensive and hypertensive. We conclude that the nonmodulat
ing trait may be a heritable defect that leads to the development of h
ypertension and is not an epiphenomenon.