Skeletal muscle afferent fibres release substance P in the nucleus tractus solitarii of anaesthetized cats.
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 microl)-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 microl)-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. 4. 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 microl)-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 microl)-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 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.
Potts
J T
JT
Department of Physiology, Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, 5323 Harry Hines boulevard, Dallas, TX 75235-9034, USA.jpotts@mednet.swmed.edu
Fuchs
I E
IE
Li
J
J
Leshnower
B
B
Mitchell
J H
JH
D000758:Anesthesia; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002415:Cats; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D008297:Male; D017551:Microdialysis; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation / Q000378:metabolism*; D009412:Nerve Fibers / Q000378:metabolism*; D009475:Neurons, Afferent / Q000378:metabolism*; D010812:Physical Stimulation; D011863:Radioimmunoassay; D017552:Solitary Nucleus / Q000166:cytology / Q000378:metabolism*; D013373:Substance P / Q000378:metabolism*
D013373:Substance P