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¢. During contraction the dialysate concentration increased 154% above resting control levels (from 0·217 ± 0·009 to 0·546 ± 0·023 fmol (100 ìl)¢, 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 ìl)¢, 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 ìl)¢ (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 ìl)¢, 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.7924

It is well documented that decrements in T4 cell and total lymphocyte counts are powerful predictors of subsequent clinical progression to AIDS. These preliminary findings suggest that life stressors and coping style may also be predictors of the development of AIDS.

SUMMARY1. 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 a-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 ul/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 St ventral roots. Basal SP-LI release was 0 20+0 03 fmol/100l ,l and was increased to 0 54 + 0-05 fmol/ 100 ,ul (mean + S.D.) by static muscle contraction. This increase was greatly attenuated after cutting the L7 and St dorsal roots (0 23 + 003 to 039 + 008 fmol/ 100 lO ) or completely abolished by muscle paralysis (027 + 0-03 to 031 + 001 fmol/l00,ul). 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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