Brief stimulation of the peroneal nerve attenuates the exercise pressor reflex in anaesthetised cats

We recently demonstrated that applying capsaicin to the common peroneal nerve, thereby activating small diameter afferent neurons, caused a substantial rise in mean arterial pressure (MAP) and heart rate (HR) that lasted approximately 20 min. In addition, this application of capsaicin transiently attenuated the exercise pressor reflex (EPR). The purpose of the current study was to test the hypothesis that stimulating the peroneal nerve at an intensity that activated both myelinated and unmyelinated axons for a short duration (1 min) causes a similar attenuation of the EPR. Cats were anaesthetised with alpha-chloralose and urethane, the popliteal fossa was exposed, and static contraction was induced by stimulating the tibial nerve. The ipsilateral peroneal nerve was cut and placed on a stimulating electrode. Prior to peroneal nerve stimulation, static contraction of the triceps surae muscle for 1 min increased MAP 48+/-8 mmHg and HR 16+/-3 bpm. Electrical stimulation of the central end of the cut peroneal nerve for 1 min (100 x motor threshold; 40 Hz; 0.1 ms) increased MAP and HR by 62+/-11 mmHg and 28+/-4 bpm, respectively. These increases returned to prestimulation levels within 1 min. Two minutes after the peroneal stimulation was stopped, the EPR was markedly reduced as muscle contraction increased MAP and HR by 20+/-4 mmHg and 7+/-2 bpm, respectively. Repeating the muscle contraction approximately 25 min after peroneal stimulation increased MAP and HR by 38+/-8 mmHg and 12+/-2 bpm, indicating some recovery of the EPR. These results show that brief (1 min) electrical stimulation of afferent neurons in the peroneal nerve attenuates the EPR. This supports the hypothesis that strong activation of small diameter afferent neurons stimulates a nervous system mechanism that diminishes the sensory input from skeletal muscle involved in cardiovascular regulation.