Nosaka S, Nakase N, Murata K
Department of Physiology, Mie University School of Medicine, Japan.
Pflugers Arch. 1989 Apr;413(6):656-66. doi: 10.1007/BF00581817.
Somatosensory and forebrain mechanisms inhibiting arterial baroreflexes were investigated in chloralose-urethane anesthetized and artificially ventilated rats. Electrical stimulation of the sciatic nerve (ScN) and the hypothalamic pressor area (HP) suppressed baroreflex vagal bradycardia (BVB) and hypotension provoked by electrical stimulation of the aortic depressor nerve (ADN). Suppression of BVB was more marked, but inhibitory potencies of ScN and HP were not different. These two inhibitions were considered to have a functional implication in common, since both were accompanied by increase in hindlimb vascular conductance. A variety of experiments were conducted to localize the target site of ScN and HP inhibitions of BVB. Either ScN or HP stimulations was without effect on antidromic compound spike potentials along ADN evoked by microstimulation of the nucleus tractus solitarius (NTS), precluding the possibility of these inhibitions being presynaptic. Both ScN and HP stimulation suppressed ADN-induced field potentials in the NA region which provoked vagal bradycardia upon microstimulation, but failed to affect ADN-induced responses, either field or unitary, in the NTS region. Antidromic unitary responses in the NA region to vagus cardiac branch stimulation were suppressed by ScN and HP stimulations in NTS-lesioned rats. Intracisternal bicuculline, a GABA antagonist, was found to abolish both ScN and HP inhibitions of BVB, while intracisternal muscimol, a GABA agonist, eliminated bradycardia. These findings suggest that somatosensory and forebrain inhibition of BVB occur principally at the preganglionic cell level and are probably mediated by a GABAergic mechanism.
在水合氯醛-乌拉坦麻醉并人工通气的大鼠中，研究了抑制动脉压力反射的躯体感觉和前脑机制。电刺激坐骨神经（ScN）和下丘脑升压区（HP）可抑制电刺激主动脉减压神经（ADN）所诱发的压力反射性迷走性心动过缓（BVB）和低血压。对BVB的抑制更为明显，但ScN和HP的抑制效力并无差异。这两种抑制被认为具有共同的功能意义，因为两者都伴随着后肢血管传导性的增加。进行了各种实验以定位ScN和HP对BVB抑制的靶点。无论是ScN还是HP刺激，对孤束核（NTS）微刺激诱发的沿ADN的逆向复合动作电位均无影响，排除了这些抑制为突触前抑制的可能性。ScN和HP刺激均抑制了NA区域中ADN诱发的场电位，该场电位在微刺激时可诱发迷走性心动过缓，但未能影响NTS区域中ADN诱发的反应，无论是场反应还是单位反应。在NTS损伤的大鼠中，ScN和HP刺激可抑制NA区域对迷走神经心脏分支刺激的逆向单位反应。发现脑池内注射GABA拮抗剂荷包牡丹碱可消除ScN和HP对BVB的抑制，而脑池内注射GABA激动剂蝇蕈醇可消除心动过缓。这些发现表明，躯体感觉和前脑对BVB的抑制主要发生在节前细胞水平，可能由GABA能机制介导。
