The direct vasodilatory and negative chronotropic effects of adenosine in humans are counterbalanced by a reflex increase in sympathetic nerve traffic. A suggested mechanism for this reflex includes peripheral chemoreceptor activation. We, therefore, assessed the contribution of carotid chemoreceptors to sympatho-excitation by adenosine. Muscle sympathetic nerve activity was recorded during adenosine infusion (140 µg·kg-1·min-1 for 5 min) in five patients lacking carotid chemoreceptors after bilateral carotid body tumour resection (one male and four female, mean age 51±11 years) and in six healthy controls (two male and four female, mean age 50±7 years). Sympathetic responses to sodium nitroprusside injections were assessed to measure baroreceptor-mediated sympathetic activation. In response to adenosine, controls showed no change in blood pressure, an increase in heart rate (+48.2±13.2%; P<0.003) and an increase in sympathetic nerve activity (+195±103%; P<0.022). In contrast, patients showed a decrease in blood pressure (-14.6±4.9/-17.6±6.0%; P<0.05), an increase in heart rate (+25.3±8.4%; P<0.032) and no significant change in sympathetic activity. Adenosine-induced hypotension in individual patients elicited less sympathetic activation than equihypotensive sodium nitroprusside injections. In humans lacking carotid chemoreceptors, adenosine infusion elicits hypotension due to the absence of significant sympatho-excitation. Chemoreceptor activation is essential for counterbalancing the direct vasodilation by adenosine. In addition, blunting of the baroreflex sympathetic response to adenosine-induced hypotension may indicate a direct sympatho-inhibitory effect of adenosine.
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Research Article|
January 01 2004
The role of carotid chemoreceptors in the sympathetic activation by adenosine in humans Available to Purchase
Henri J. L. M. TIMMERS;
*Department of General Internal Medicine, University Medical Center Nijmegen, PO Box 9101, 6500 HB Nijmegen, The Netherlands
Correspondence: Dr Henri J. L. M. Timmers (e-mail [email protected]).
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Gerard A. RONGEN;
Gerard A. RONGEN
*Department of General Internal Medicine, University Medical Center Nijmegen, PO Box 9101, 6500 HB Nijmegen, The Netherlands
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John M. KAREMAKER;
John M. KAREMAKER
†Department of Physiology, Academic Medical Center, PO Box 22660, 1100DD Amsterdam, The Netherlands
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Wouter WIELING;
Wouter WIELING
‡Department of Internal Medicine, Academic Medical Center, PO Box 22660, 1100DD Amsterdam, The Netherlands
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Henri A. M. MARRES;
Henri A. M. MARRES
§Department of Otorhinolaryngology, University Medical Center Nijmegen, PO Box 9101, 6500 HB Nijmegen, The Netherlands
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Jacques W. M. LENDERS
Jacques W. M. LENDERS
*Department of General Internal Medicine, University Medical Center Nijmegen, PO Box 9101, 6500 HB Nijmegen, The Netherlands
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Publisher: Portland Press Ltd
Received:
May 13 2003
Revision Received:
July 29 2003
Accepted:
August 22 2003
Accepted Manuscript online:
August 22 2003
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2004 The Biochemical Society
2004
Clin Sci (Lond) (2004) 106 (1): 75–82.
Article history
Received:
May 13 2003
Revision Received:
July 29 2003
Accepted:
August 22 2003
Accepted Manuscript online:
August 22 2003
Citation
Henri J. L. M. TIMMERS, Gerard A. RONGEN, John M. KAREMAKER, Wouter WIELING, Henri A. M. MARRES, Jacques W. M. LENDERS; The role of carotid chemoreceptors in the sympathetic activation by adenosine in humans. Clin Sci (Lond) 1 January 2004; 106 (1): 75–82. doi: https://doi.org/10.1042/CS20030174
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