HEART-RATE AND BLOOD-PRESSURE VARIABILITIES IN SALT-SENSITIVE HYPERTENSION

Citation
G. Piccirillo et al., HEART-RATE AND BLOOD-PRESSURE VARIABILITIES IN SALT-SENSITIVE HYPERTENSION, Hypertension, 28(6), 1996, pp. 944-952
Citations number
29
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0194911X
Volume
28
Issue
6
Year of publication
1996
Pages
944 - 952
Database
ISI
SICI code
0194-911X(1996)28:6<944:HABVIS>2.0.ZU;2-V
Abstract
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.