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(Hypertension. 1996;28:944-952.)
© 1996 American Heart Association, Inc.

Articles

Heart Rate and Blood Pressure Variabilities in Salt-Sensitive Hypertension

Gianfranco Piccirillo; Carmela Bucca; Michele Durante; Elvira Santagada; Maria R. Munizzi; Mauro Cacciafesta; Vincenzo Marigliano

I Clinica Medica, Policlinico Umberto I, Universita "La Sapienza," Rome, Italy.

Correspondence to Dr Gianfranco Piccirillo, I Clinica Medica, Policlinico Umberto I, 00161 Rome, Italy.

In salt-sensitive hypertension, a high sodium intake causes plasma catecholamines 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 variabilities and baroreceptor sensitivity. In all subjects, high sodium intake significantly enhanced the low-frequency power of heart rate and arterial pressures at rest and after sympathetic stress. It also increased heart rate and arterial pressure variabilities. During high sodium intake, salt-sensitive hypertensive subjects had significantly higher low-frequency powers of systolic arterial pressure (7.5 mm Hg², P<.05) and of heart rate at rest (59.2±2.4 normalized units [NU], P<.001) than salt-resistant subjects (6.6±0.3 mm Hg², 55.0±3.2 NU) and normotensive control subjects (5.1±0.5 mm Hg², 41.6±2.9 NU). In salt-sensitive subjects, low sodium intake significantly reduced low-frequency normalized units (P<.001) and the ratio of low- to high-power frequency (P<.001). High-sodium intake significantly increased 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 markedly enhances cardiac sympathetic activity in salt-sensitive and salt-resistant hypertension. In contrast, although reduced sodium intake lowers arterial pressure and sympathetic activity, it does so only in salt-sensitive subjects. Hence, in salt-resistant subjects, neither arterial pressure nor sympathetic activity depends on salt intake. During a high sodium intake in normotensive subjects and salt-resistant hypertensive subjects, increased sympathetic activity is probably compensated by enhanced baroreflex sensitivity.

Key Words: autonomic nervous system • sodium • hypertension, sodium-dependent • baroreflex • norepinephrine

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