1. The purpose of this study was to determine if static skeletal muscle contraction causes the release of substance P(SP) in the L7‐dorsal horn region of the spinal cord. A laminectomy was performed to expose the spinal cord of alpha‐chloralose anaesthetized cats. The L6 spinal root was cut. A microdialysis probe was inserted into the L7 dorsal horn region ipsilateral to the contracting triceps surae muscle. The probe was perfused with a buffer solution at 3 microliters/min. Substance P‐like immunoreactivity (SP‐LI) was measured, from the microdialysis samples, by radioimmunoassay. 2. A 5‐9 min contraction of the triceps surae muscle was evoked by alternate electrical stimulation of the peripheral ends of the cut L7 and S1 ventral roots. Basal SP‐LI release was 0.20 +/‐ 0.03 fmol/100 microliters and was increased to 0.54 +/‐ 0.05 fmol/100 microliters (mean +/‐ S.D.) by static muscle contraction. This increase was greatly attenuated after cutting the L7 and S1 dorsal roots (0.23 +/‐ 0.03 to 0.39 +/‐ 0.08 fmol/100 microliters) or completely abolished by muscle paralysis (0.27 +/‐ 0.03 to 0.31 +/‐ 0.01 fmol/100 microliters). Muscle contraction also increased mean arterial blood pressure (MAP) 29 +/‐ 20 mmHg and heart rate (HR) 11 +/‐ 5 beats/min (mean +/‐ S.D.). These cardiovascular changes to muscle contraction were abolished by sectioning the dorsal roots or when the ventral roots were electrically stimulated after the cats were paralysed. 3. These results demonstrate that static contraction of skeletal muscle increases the release of SP‐LI in the dorsal horn of the spinal cord. Furthermore, these data support the hypothesis that SP plays a role in mediating the cardiovascular responses evoked during static exercise.
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