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. 2. 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). 3. 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. 5. 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 cNTB. 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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