In salt-sensitive hypertension, a high sodium intake causes plasma cat
echolamines to rise and pulmonary baroreceptor plasticity to fall. In
salt-sensitive and salt-resistant hypertensive subjects during low and
high sodium intakes, we studied autonomic nervous system activity by
power spectral analysis of heart rate and arterial pressure variabilit
ies and baroreceptor sensitivity. Tn lah subjects, high sodium intake
significantly enhanced the low-frequency power of heart rate and arter
ial pressures at rest and after sympathetic stress. It also increased
hart rate and arterial pressure variabilities. During high sodium inta
ke, salt-sensitive hypertensive subjects had significantly higher low-
frequency powers of systolic arterial pressure (7.5 mm Hg-2, P < .05)
and of heart rate at rest (59.2 +/- 2.4 normalized units [NU], P < .00
1) than salt-resistant subjects (6.6 +/- 0.3 mm Hg-2, 55.0 +/- 3.2 NU)
and normotensive control subjects (5.1 +/- 0.5 mm Hg-2, 41.6 +/- 2.9
NU). In salt-sensitive subjects, low sodium intake significantly reduc
ed low-frequency normalized units (P < .001) and the ratio of low- to
high-power frequency (P < .001). High-sodium intake significantly incr
eased baroreflex sensitivity in control subjects (from 10.0 +/- 0.7 to
17.5 +/- 0.7 ms/mm Hg, P < .001) and salt-resistant subjects (from 6.
9 +/- 0.7 to 13.9 +/- 0.9, P < .05) but not in salt-sensitive subjects
(7.4 +/- 0.3 to 7.9 +/- 0.4). In conclusion, a high sodium intake mar
kedly enhances cardiac sympathetic activity in salt-sensitive and salt
-resistant hypertension In contrast, although reduced sodium intake lo
wers arterial pressure and sympathetic activity, it does so only in sa
lt-sensitive subjects. Hence, in salt-resistant subjects, neither arte
rial pressure nor sympathetic activity depends on salt intake. During
a high sodium intake in normotensive subjects and salt-resistant hyper
tensive subjects, increased sympathetic activity is probably compensat
ed by enhanced baroreflex sensitivity.