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1 Hypertension Clinic, Erasme Hospital, 1070 Brussels, Belgium; 2 Centro Ricerche Cardiovascolari, Medicina Interna II, Ospedale L. Sacco, Università degli studi di Milano, 20157 Milano, Italy; 3 Department of Hypertension and Diabetology, Medical University of Gdansk, 80-158 Gdansk, Poland; and 4 Divisions of Hypertension and Cardiology, Mayo Clinic, Rochester, Minnesota 55902
Interactions between
mechanisms governing ventilation and blood pressure (BP) are not well
understood. We studied in 11 resting normal subjects the effects of
sustained isocapnic hyperventilation on arterial baroreceptor
sensitivity, determined as the
index between oscillations in
systolic BP (SBP) generated by respiration and oscillations present in
R-R intervals (RR) and in peripheral sympathetic nerve traffic [muscle
sympathetic nerve activity (MSNA)]. Tidal volume increased from
478 ± 24 to 1,499 ± 84 ml and raised SBP from 118 ± 2 to 125 ± 3 mmHg, whereas RR decreased from 947 ± 18 to
855 ± 11 ms (all P < 0.0001); MSNA did not
change. Hyperventilation reduced arterial baroreflex sensitivity to
oscillations in SBP at both cardiac (from 13 ± 1 to 9 ± 1 ms/mmHg, P < 0.001) and MSNA levels (by
37 ± 5%, P < 0.0001). Thus increased BP during hyperventilation
does not elicit any reduction in either heart rate or MSNA. Baroreflex
modulation of RR and MSNA in response to hyperventilation-induced BP
oscillations is attenuated. Blunted baroreflex gain during
hyperventilation may be a mechanism that facilitates simultaneous
increases in BP, heart rate, and sympathetic activity during dynamic
exercise and chemoreceptor activation.
ventilation; sinus node
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