Penn State Heart and Vascular Institute, 500 University Dr., Mail Code H047, Hershey Medical Center, Hershey, PA 17033, USA.
Am J Physiol Heart Circ Physiol. 2010 Aug;299(2):H557-65. doi: 10.1152/ajpheart.00387.2010. Epub 2010 Jun 11.
Recently, opioid receptors have been shown to be expressed on group III and IV afferents, which comprise the sensory arm of the exercise pressor reflex. Although the stimulation of opioid receptors in the central nervous system has been shown to attenuate the exercise pressor reflex, the effect on the reflex of their stimulation in the periphery is unknown. We therefore tested the hypothesis that the activation of peripheral mu-opioid receptors attenuates the exercise pressor reflex. The pressor responses to static contraction were compared before and after the injection of the mu-opioid receptor agonist [d-Ala(2),N-MePhe(4),Gly-ol(5)]enkephalin (DAMGO; 1 microg) into the abdominal aorta of decerebrated rats in which one femoral artery had been occluded 72 h previously (n = 10) and in control rats whose femoral arteries were freely perfused (n = 8). DAMGO attenuated the peak pressor response to contraction in rats whose femoral arteries had been occluded (before: increase of 34 + or - 3 mmHg and after: increase of 22 + or - 2 mmHg, P = 0.008); the inhibitory effect of DAMGO was prevented by the injection of naloxone (100 microg) into the abdominal aorta (before: increase of 29 + or - 5 mmHg and after: increase of 29 + or - 5 mmHg, P = 0.646, n = 7). An intravenous injection of DAMGO (1 microg, n = 6) had no effect on the peak pressor response to contraction in both groups of rats. DAMGO had no effect on the peak pressor response to contraction in rats whose femoral arteries were freely perfused (before: Delta 23 + or - 4 mmHg, after: Delta 23 + or - 3 mmHg, n = 6) but appeared to have a small effect on topography of the response. DAMGO had no effect on the peak pressor response to tendon stretch in both groups of rats (both P > 0.05). We conclude that the stimulation of peripheral mu-opioid receptors attenuates the exercise pressor reflex in rats whose femoral arteries have been ligated for 72 h.
最近,已经证明阿片受体存在于 III 组和 IV 组传入纤维上,这些传入纤维构成运动性加压反射的感觉臂。虽然中枢神经系统中阿片受体的刺激已被证明可以减弱运动性加压反射,但外周刺激对反射的影响尚不清楚。因此,我们假设外周 μ 阿片受体的激活可以减弱运动性加压反射。在预先阻断股动脉 72 小时的去大脑大鼠(n = 10)和股动脉自由灌注的对照组大鼠(n = 8)中,比较了在腹主动脉内注射 μ 阿片受体激动剂 [d-Ala(2),N-MePhe(4),Gly-ol(5)]-脑啡肽(DAMGO;1 μg)前后的静态收缩压反应。DAMGO 减弱了股动脉闭塞大鼠的收缩压峰值反应(前:增加 34 ± 3 mmHg,后:增加 22 ± 2 mmHg,P = 0.008);DAMGO 的抑制作用可通过向腹主动脉内注射纳洛酮(100 μg)来预防(前:增加 29 ± 5 mmHg,后:增加 29 ± 5 mmHg,P = 0.646,n = 7)。静脉注射 DAMGO(1 μg,n = 6)对两组大鼠的收缩压峰值反应均无影响。DAMGO 对股动脉自由灌注大鼠的收缩压峰值反应无影响(前:Δ23 ± 4 mmHg,后:Δ23 ± 3 mmHg,n = 6),但似乎对反应的形态有轻微影响。DAMGO 对两组大鼠的肌腱拉伸的最大加压反应均无影响(均 P > 0.05)。我们的结论是,在股动脉结扎 72 小时的大鼠中,外周 μ 阿片受体的刺激可以减弱运动性加压反射。