TY - JOUR
T1 - Attenuation of reflex pressor and ventilatory responses to static muscular contraction by intrathecal opioids
AU - Hill, J. M.
AU - Kaufman, M. P.
PY - 1990
Y1 - 1990
N2 - We have tested the hypothesis that intrathecal injections of opioid peptides attenuate the reflex pressor and ventilatory responses to static contraction of the triceps surae muscles of chloralose-anesthetized cats. We found that before intrathecal injections of [D-Ala2]Met-enkephalinamide (100 μg in 0.2 ml), static contraction increased mean arterial pressure and ventilation by 32 ± 5 (SE) mmHg and 227 ± 61 (SE) ml/min, whereas after injection of this opioid peptide, static contraction increased mean arterial pressure and ventilation by only 15 ± 5 mmHg and 37 ± 33 ml/min, respectively. The attenuation of both the pressor and ventilatory responses to static contraction by [D-Ala2]Met-enkephalinamide were statistically significant (P < 0.05). Moreover, the attenuation was probably not caused by an opioid-induced withdrawal of sympathetic outflow because [D-Ala2]Met-enkephalinamide had no effect on the pressor and ventilatory responses evoked by high-intensity electrical stimulation of the central cut end of the sciatic nerve. In addition, intrathecal injection of peptides that were highly selective agonists for either the opioid μ- or δ-receptor attenuated the reflex response to static contraction. Naloxone (1,000 μg), injected intrathecally, prevented the attenuation of the reflex responses to contraction by opioid peptides. We speculate that the opioid-induced attenuation of the reflex pressor and ventilatory responses to static contraction may have been due to suppression of substance P release from group III and IV muscle afferents.
AB - We have tested the hypothesis that intrathecal injections of opioid peptides attenuate the reflex pressor and ventilatory responses to static contraction of the triceps surae muscles of chloralose-anesthetized cats. We found that before intrathecal injections of [D-Ala2]Met-enkephalinamide (100 μg in 0.2 ml), static contraction increased mean arterial pressure and ventilation by 32 ± 5 (SE) mmHg and 227 ± 61 (SE) ml/min, whereas after injection of this opioid peptide, static contraction increased mean arterial pressure and ventilation by only 15 ± 5 mmHg and 37 ± 33 ml/min, respectively. The attenuation of both the pressor and ventilatory responses to static contraction by [D-Ala2]Met-enkephalinamide were statistically significant (P < 0.05). Moreover, the attenuation was probably not caused by an opioid-induced withdrawal of sympathetic outflow because [D-Ala2]Met-enkephalinamide had no effect on the pressor and ventilatory responses evoked by high-intensity electrical stimulation of the central cut end of the sciatic nerve. In addition, intrathecal injection of peptides that were highly selective agonists for either the opioid μ- or δ-receptor attenuated the reflex response to static contraction. Naloxone (1,000 μg), injected intrathecally, prevented the attenuation of the reflex responses to contraction by opioid peptides. We speculate that the opioid-induced attenuation of the reflex pressor and ventilatory responses to static contraction may have been due to suppression of substance P release from group III and IV muscle afferents.
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U2 - 10.1152/jappl.1990.68.6.2466
DO - 10.1152/jappl.1990.68.6.2466
M3 - Article
C2 - 2384427
AN - SCOPUS:0025299969
SN - 0161-7567
VL - 68
SP - 2466
EP - 2472
JO - Journal of applied physiology
JF - Journal of applied physiology
IS - 6
ER -