Normotensive salt sensitivity, a putative precursor of hypertension, might
be quite frequent in African Americans (blacks) and less frequent in Caucas
ian Americans (whites), but only when dietary potassium is deficient and no
t when maintained well within the normal range. We tested this hypothesis i
n 41 metabolically controlled studies of 38 healthy normotensive men (24 bl
acks, 14 whites) who ate a basal diet low in sodium (15 mmol/d) and margina
lly deficient in potassium (30 mmol/d) for 6 weeks. Throughout the last 4 w
eeks, NaCl was loaded (250 mmol/d); throughout the last 3, potassium was su
pplemented (as potassium bicarbonate) to either mid- or high-normal levels,
70 and 120 mmol/d. Salt sensitivity, defined as an increase in mean arteri
al blood pressure greater than or equal to 3 mm Hg with salt loading, was d
eemed "moderate" if increasing less than or equal to 10 mm Hg and "severe"
if increasing mere. When dietary potassium was 30 mmol/d, salt loading indu
ced a mean increase in blood pressure only in blacks (P<0.001), and salt se
nsitivity occurred in most blacks but not whites (79% vs 36% (P<0.02). Supp
lementing potassium only to 70 mmol/d attenuated moderate salt sensitivity
similarly in blacks and whites; 120 mmol/d abolished it, attenuated severe
salt sensitivity, which occurred in a quarter of affected blacks, and suppr
essed the frequency and severity of salt sensitivity in blacks to levels si
milar to those observed in whites. These observations demonstrate that in m
ost normotensive black men but not white men, salt sensitivity occurs when
dietary potassium is even marginally deficient but is dose-dependently supp
ressed when dietary potassium is increased within its normal range. Such su
ppression might prevent or delay the occurrence of hypertension, particular
ly in the many blacks, in whom dietary potassium is deficient.