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Blockade of acid sensing ion channels attenuates the augmented exercise pressor reflex in rats with chronic femoral artery occlusion
Author(s) -
Tsuchimochi Hirotsugu,
Yamauchi Katsuya,
McCord Jennifer L.,
Kaufman Marc P.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.217851
Subject(s) - medicine , femoral artery , reflex , hindlimb , peripheral , cardiology , blood pressure , blood flow , contraction (grammar) , skeletal muscle , artery , stimulation , anesthesia
Non‐technical summary In patients with peripheral artery disease arterial blood flow to the legs is adequate at rest, but does not increase to meet metabolic demand of the muscles during exercise. Consequently, the arterial blood pressure response to exercise in these patients is greater than it is in healthy subjects. We tested the hypothesis that this exaggerated arterial pressure response to exercise is caused by the stimulation of the ion channel ASIC3 on the endings of sensory nerves in contracting skeletal muscle. We performed our experiments in decerebrated rats. Three days before the experiment, we ligated the left femoral artery, a manoeuvre which has been shown to simulate the arterial blood flow patterns to hindlimb skeletal muscles that are found in patients with peripheral artery disease. We found that blockade of ASIC3 with two different compounds attenuated the increase in arterial pressure evoked by left hindlimb muscle contraction.