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Research Article Free access | 10.1172/JCI114916

Arterial baroreflex buffering of sympathetic activation during exercise-induced elevations in arterial pressure.

U Scherrer, S L Pryor, L A Bertocci, and R G Victor

Department of Internal Medicine, (Cardiology Division), Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Scherrer, U. in: PubMed | Google Scholar

Department of Internal Medicine, (Cardiology Division), Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Pryor, S. in: PubMed | Google Scholar

Department of Internal Medicine, (Cardiology Division), Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Bertocci, L. in: PubMed | Google Scholar

Department of Internal Medicine, (Cardiology Division), Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Victor, R. in: PubMed | Google Scholar

Published December 1, 1990 - More info

Published in Volume 86, Issue 6 on December 1, 1990
J Clin Invest. 1990;86(6):1855–1861. https://doi.org/10.1172/JCI114916.
© 1990 The American Society for Clinical Investigation
Published December 1, 1990 - Version history
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Abstract

Static muscle contraction activates metabolically sensitive muscle afferents that reflexively increase sympathetic nerve activity and arterial pressure. To determine if this contraction-induced reflex is modulated by the sinoaortic baroreflex, we performed microelectrode recordings of sympathetic nerve activity to resting leg muscle during static handgrip in humans while attempting to clamp the level of baroreflex stimulation by controlling the exercise-induced rise in blood pressure with pharmacologic agents. The principal new finding is that partial pharmacologic suppression of the rise in blood pressure during static handgrip (nitroprusside infusion) augmented the exercise-induced increases in heart rate and sympathetic activity by greater than 300%. Pharmacologic accentuation of the exercise-induced rise in blood pressure (phenylephrine infusion) attenuated these reflex increases by greater than 50%. In contrast, these pharmacologic manipulations in arterial pressure had little or no effect on: (a) forearm muscle cell pH, an index of the metabolic stimulus to skeletal muscle afferents; or (b) central venous pressure, an index of the mechanical stimulus to cardiopulmonary afferents. We conclude that in humans the sinoaortic baroreflex is much more effective than previously thought in buffering the reflex sympathetic activation caused by static muscle contraction.

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