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Physiological and Molecular Mechanisms Implicated in the Neural Control of Circulation

Platelet inhibition by low-dose aspirin but not by clopidogrel reduces the axon-reflex current-induced vasodilation in humans

¹Laboratory of Vascular Investigations, ²Laboratory of Haemostasis University Hospital of Angers, France, ³Integrative Neurovascular Biology, UMR Centre National de la Recherche Scientifique (CNRS) 6214 - Institut National de la Santé et de la Recherche Médicale 771, Medical School, University of Angers, France; and ⁴Neurovascular Interactions Formation de Recherche en Evolution CNRS 3075, University of Lyon 1, France

Submitted 7 November 2007 ; accepted in final form 2 February 2008

We previously showed a prolonged inhibition of current-induced vasodilation (CIV) after a single oral high dose of aspirin. In this study, we tested the hypothesis of platelet involvement in CIV. Nine healthy volunteers took 75 mg aspirin/day, 98 mg of clopidogrel bisulfate/day, or placebo for 4 days. CIV was induced by two consecutive 1-min anodal current applications (0.08 mA/cm²) through deionized water with a 10-min interval. CIV was measured with laser Doppler flowmetry and expressed as a percentage of baseline cutaneous vascular conductance: %C_b. In a second experiment in 10 volunteers, aspirin and placebo were given as in experiment 1, but a 26-h delay from the last aspirin intake elapsed before ACh iontophoresis and postocclusive hyperemia were studied in parallel to CIV. In experiment 1, the means ± SE amplitude of CIV was 822 ± 314, 313 ± 144, and 746 ± 397%C_b with placebo, aspirin (P < 0.05 from placebo and clopidogrel), and clopidogrel (NS from placebo), respectively. In experiment 2, CIV impairment with aspirin was confirmed: CIV amplitudes were 300 ± 99, and 916 ± 528%C_b under aspirin and placebo, respectively (P < 0.05), whereas vasodilation to ACh iontophoresis (322 ± 74 and 365 ± 104%C_b) and peak postocclusive hyperemia (491 ± 137 and 661 ± 248%C_b) were not different between aspirin and placebo, respectively. Low-dose aspirin, even 26 h after oral administration, impairs CIV, while ACh-mediated vasodilation and postocclusive hyperemia are preserved. If platelets are involved in the neurovascular mechanism triggered by galvanic current application in humans, it is likely to occur through the cyclooxygenase but not the ADP pathway.

microcirculation; axon reflex; platelets; skin

This article has been cited by other articles:

				G. Mahe, P. Rousseau, J. L. Saumet, and P. Abraham About "Chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilatation in middle-aged humans" J Appl Physiol, April 1, 2009; 106(4): 1471 - 1471. [Full Text] [PDF]

				L. A. Holowatz and W. L. Kenney Chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilation in middle-aged humans J Appl Physiol, February 1, 2009; 106(2): 500 - 505. [Abstract] [Full Text] [PDF]