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Am J Physiol Heart Circ Physiol 279: H536-H541, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 2, H536-H541, August 2000

Hyperventilation alters arterial baroreflex control of heart rate and muscle sympathetic nerve activity

Philippe Van de Borne1, Silvia Mezzetti2, Nicola Montano2, Krzysztof Narkiewicz3, Jean Paul Degaute1, and Virend K. Somers4

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 alpha  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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