Nóbrega A C, Meintjes A F, Ally A, Wilson L B
Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas 75235, USA.
Am J Physiol. 1995 Apr;268(4 Pt 2):H1577-85. doi: 10.1152/ajpheart.1995.268.4.H1577.
This study investigated whether activation of serotonin1A [5-hydroxytryptamine (5-HT)1A] receptors in the dorsal horn of the spinal cord attenuates the reflex pressor response to static contraction and passive muscle stretch. In addition, we determined if the attenuation of the response to contraction is mediated by inhibiting substance P (SP) release in the dorsal horn. Static contractions of the triceps surae muscle of chloralose-anesthetized cats were induced by stimulating the cut L7 and S1 ventral roots. Microdialysis (10 mM) of a selective 5-HT1A agonist [8-hydroxy-2-(di-N-propylamino)tetralin (8-OH-DPAT)] into the L7 dorsal horn region produced a reversible attenuation of the reflex pressor response to a 1-min contraction (in mmHg: control = 36 +/- 3; 8-OH-DPAT = 17 +/- 3; recovery = 31 +/- 8; P = 0.013; n = 6) or passive stretch (in mmHg: control = 36 +/- 6; 8-OH-DPAT = 15 +/- 2; recovery = 32 +/- 6; P = 0.002; n = 6). However, a 5-HT1B agonist, 1-[3-(trifluoromethyl)-phenyl]piperazine, had no effect on the reflex pressor response. During 5-min contractions (n = 8), 8-OH-DPAT (10 mM) also blunted the pressor response but had no effect on the levels of SP-like immunoreactivity (in fmol/100 microliters: control = 0.492 +/- 0.026; 8-OH-DPAT = 0.501 +/- 0.034). These results suggest that activation of 5-HT1A receptors in the dorsal horn attenuates the reflex pressor response to contraction through a mechanism other than inhibition of SP release.
本研究调查了脊髓背角中5-羟色胺1A（5-HT1A）受体的激活是否会减弱对静态收缩和被动肌肉拉伸的反射性升压反应。此外，我们还确定了对收缩反应的减弱是否是通过抑制背角中P物质（SP）的释放来介导的。通过刺激氯醛糖麻醉猫的L7和S1腹侧神经根，诱发其腓肠肌的静态收缩。将选择性5-HT1A激动剂[8-羟基-2-（二-N-丙基氨基）四氢萘（8-OH-DPAT）]（10 mM）微透析至L7背角区域，可使对1分钟收缩（以毫米汞柱计：对照组=36±3；8-OH-DPAT组=17±3；恢复组=31±8；P=0.013；n=6）或被动拉伸（以毫米汞柱计：对照组=36±6；8-OH-DPAT组=15±2；恢复组=32±6；P=0.002；n=6）的反射性升压反应产生可逆性减弱。然而，5-HT1B激动剂1-[3-（三氟甲基）-苯基]哌嗪对反射性升压反应没有影响。在5分钟收缩期间（n=8），8-OH-DPAT（10 mM）也减弱了升压反应，但对SP样免疫反应性水平没有影响（以飞摩尔/100微升计：对照组=0.492±0.026；8-OH-DPAT组=0.501±0.034）。这些结果表明，背角中5-HT1A受体的激活通过一种不同于抑制SP释放的机制减弱了对收缩的反射性升压反应。
