Key result
B2 antagonist HOE 140 reduces noradrenaline spillover ~68% during canine muscle contraction.
Bradykinin formation during muscle contraction facilitates noradrenaline spillover via B2 receptors in the canine gracilis muscle.
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B2 blockade attenuates spillover in canine contracting muscle; leaves open bradykinin-B2 modulation of sympathetic activity in human exercise.
Noradrenaline spillover from skeletal muscle vascular areas increases during exercise but the underlying mechanisms are not well understood. Muscle contraction itself causes changes in many factors that could affect noradrenaline spillover. For instance, it has been reported that bradykinin is synthesized in skeletal muscle areas during contraction. Because the B2 bradykinin receptor facilitates noradrenaline spillover, it may be involved in the increase associated with contraction. In this experiment, we studied the effect of bradykinin on noradrenaline spillover in the in situ canine gracilis muscle, using the specific B2 antagonist HOE 140. The drug did not modify noradrenaline spillover at rest, but did cause a significant decrease during muscle contraction, from 558 to 181 pg min(-1). As reported previously in the literature, fractional extraction of noradrenaline decreased during muscle contraction. This effect was independent of HOE 140 treatment. In light of our results, it seems that bradykinin formation during muscle contraction may play an important part in the observed increase in noradrenaline spillover but does not affect fractional extraction.
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Lavoie et al. (2001) studied this question. HOE 140 was evaluated on Noradrenaline spillover during muscle contraction. Administration of the B2 antagonist HOE 140 significantly decreased noradrenaline spillover during muscle contraction from 558 to 181 pg min(-1) in the canine gracilis muscle.
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