CARDIOVASCULAR AUTONOMIC MODULATION IN ESSENTIAL-HYPERTENSION - EFFECT OF TILTING

To better understand the role played by the autonomic nervous system in essential hypertension, we used autoregressive power spectrum analysis to study the noncasual oscillations in RR interval, blood pressure, and skin blood flow in 40 subjects with mild to moderate hypertension and in 25 age-matched control subjects at low frequency (index of sympathetic activity to the heart and the peripheral circulation) and high frequency, respiratory related (index of vagal tone to the heart): RR interval, respiration, noninvasive systolic blood pressure, and skin arteriolar blood flow were simultaneously and continuously recorded with subjects in the supine position and immediately after tilting. The low-frequency component was not significantly different in the two groups either at the cardiac level (control versus hypertensive subjects: 39.1+/-4.3 versus 39.9+/-3.7 normalized units [NU]) or at the vascular level (152+/-0.17 versus 1.69+/-0.13 ln mm Hg-2). After head-up tilting, the RR interval fluctuations were less in hypertensive subjects (low-frequency components from 39.9+/-3.7 to 48.4+/-4.1 NU, P<.05; high-frequency components from 53.9+/-3.7 to 44+/-4 NU, P<.05) than in control subjects (low-frequency components from 39.1+/-4.3 to 64.4+/-4.9 NU, P<.001; high-frequency components from 56.0+/-4.5 to 31.2+/-4.6 NU, P<.001); the low-frequency components in systolic blood pressure increased similarly in hypertensive subjects (to 2.43+/-0.17 ln mm Hg-2, P<.0001) and in control subjects (to 2.44+/-0.21 ln mm Hg-2, P<.01), but the low-frequency components in skin blood flow increased only in control subjects (from 5.34+/-0.45 to 6.55+/-0.53 mm Hg-2, P<.01), not in hypertensive subjects (from 5.55+/-0.34 to 5.60+/-0.35 ln mm Hg-2). In hypertensive subjects with left ventricular hypertrophy, the low-frequency components in systolic blood pressure did not increase after tilting (from 1.75+/-0.33 to 2.05+/-0.41 ln mm Hg-2). Baroreflex sensitivity, as assessed by spectrum analysis, was significantly lower in hypertensive than in control subjects (5.17+/-0.49 versus 13.18+/-2.44 ms/mm Hg, P<.001). Power spectrum analysis did not reveal an increased sympathetic activity or reactivity either at the cardiac or at the vascular level. The decreased baroreceptor sensitivity in hypertensive subjects could explain the reduced change in sympathovagal balance in the tilt position at the cardiac level. In hypertensive subjects without left ventricular hypertrophy, cardiopulmonary reflex deactivation induced by tilting and/or amplification of sympathetic nervous tone by arteriolar structural change could have preserved the sympathetic activation at the vascular level.