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Bradykinin B2 Receptor Contributes to the Exaggerated Muscle Mechanoreflex in Rats with Femoral Artery Occlusion.

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Bradykinin B2 Receptor Contributes to the Exaggerated Muscle Mechanoreflex in Rats with Femoral Artery Occlusion.

Am J Physiol Heart Circ Physiol. 2013 Feb 15;

Authors: Lu J, Xing J, Li J

Muscle contraction activates the exercise pressor reflex which increases sympathetic nerve activity (SNA) and blood pressure (BP). Bradykinin (BK) is considered as a muscle metabolite responsible for modulation of the sympathetic and cardiovascular responses to contraction. Prior studies have suggested that kinin B2 receptor mediates the effects of BK on the reflex SNA and BP responses during stimulation of skeletal muscle afferents. In peripheral artery disease, amplified SNA and BP responses to exercise were observed. This dysfunction of the exercise pressor reflex is mediated, in part, by muscle mechanoreflex overactivity. Thus, we determined if B2 receptor contributes to the augmented mechanoreflex activity in rats with 24 hrs of femoral ligation. First, our data show that B2 displays significant over-expression in dorsal root ganglion of ligated limbs as compared with control limbs. Second, mechanoreflex was evoked by passive tendon stretch and the reflex SNA and BP responses to stretch were examined after HOE-140, a B2 receptors blocker, was arterially injected into the hindlimb muscles. The results demonstrate that the stretch evoked-reflex responses were attenuated by HOE-140 in control rats and ligated rats; however, the attenuating effects of HOE-140 were significantly greater in ligated rats. In contrast, there is no significant difference in B1 expression in both groups, and arterial injection of R-715, a B1 receptors blocker, had no significant effects on RSNA and MAP responses evoked by stretch. Accordingly, our data support the hypothesis that heightened B2 expression in the sensory nerves contributes to the exaggerated muscle mechanoreflex in hindlimb ischemia.

PMID: 23417862 [PubMed – as supplied by publisher]

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