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Skeletal muscle afferent fibres release substance P in the nucleus tractus solitarii of anaesthetized cats

Jeffrey T. Potts *, Ingbert E. Fuchs ¹, Jianhua Li ¹, Bradley Leshnower ¹ and Jere H. Mitchell *¹

The tachykinin substance P was recovered from the commissural subdivision of the nucleus tractus solitarii (cNTS) using in vivo microdialysis during activation of cardiorespiratory and skeletal muscle receptors in thirteen chloralose-anaesthetized cats.

Tetanic muscle contraction was evoked by stimulating L7-S1 ventral roots (n = 7). Electrically induced muscle contraction increased mean arterial pressure (MAP) by 55 ± 10 mmHg and heart rate by 29 ± 6 beats min^-1. During contraction the dialysate concentration increased 154 % above resting control levels (from 0·217 ± 0·009 to 0·546 ± 0·023 fmol (100 µl)^-1, control vs. contraction, P < 0·05).

Loss of cardiorespiratory input following disruption of the carotid sinus and vagus nerves significantly blunted, but did not abolish, the increase in substance P during muscle contraction (from 0·247 ± 0·022 to 0·351 ± 0·021 fmol (100 µl)^-1, control vs. contraction, P < 0·05). Approximately 44 % of the substance P release during contraction was independent of cardiorespiratory input transmitted by carotid sinus and vagus nerves.

To determine the contribution of cardiorespiratory related neural input on substance P release, an intravascular balloon positioned in the thoracic aorta was inflated to increase arterial pressure (n = 6). Balloon inflation increased MAP by 50 ± 5 mmHg and substance P increased from 0·251 ± 0·025 to 0·343 ± 0·028 fmol (100 µl)^-1 (control vs. balloon inflation, P < 0·05). This increase was completely abolished following interruption of vagal and carotid sinus nerves (from 0·301 ± 0·012 to 0·311 ± 0·014 fmol (100 µl)^-1, control vs. balloon inflation). This finding shows that neural input from cardiorespiratory receptors (primarily arterial baroreceptors) accounted for 37 % of the total substance P release during muscle contraction.

The findings from this study demonstrate that activation of skeletal muscle receptors and cardiorespiratory receptors (predominantly arterial baroreceptors) increases the extraneuronal concentration of substance P in the cNTS. Because substance P release was not completely abolished during muscle contraction following disruption of carotid sinus and vagus nerves it is proposed that: (1) afferent projections from contraction-sensitive skeletal muscle receptors may release substance P in the NTS; (2) neural input from muscle receptors activates substance P-containing neurones within the NTS; and (3) convergence of afferent input from skeletal muscle receptors and arterial baroreceptors onto substance P-containing neurones in the cNTS facilitates the release of substance P. The role of tachykininergic modulation of cardiorespiratory input is discussed.

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