Schneider C, Singewald N, Philippu A
Institut für Pharmakologie und Toxikologie, Universität Innsbruck, Austria.
Naunyn Schmiedebergs Arch Pharmacol. 1995 Sep;352(3):291-6. doi: 10.1007/BF00168559.
We have previously shown that experimentally induced blood pressure changes modify the release rates of catecholamines in the hypothalamus and the locus coeruleus. The aim of the present investigation was to identify the peripheral baroreceptors and the centripetal pathways responsible for the changes of catecholamine release in these brain areas. In anaesthetized cats, push-pull cannulae were bilaterally inserted into the locus coeruleus and the posterior hypothalamus. The two brain areas were superfused simultaneously with artificial cerebrospinal fluid. Baroreceptor activation by phenylephrine-induced blood pressure elevation decreased the release rate of noradrenaline in the locus coeruleus and the release rates of noradrenaline and dopamine in the posterior hypothalamus. Similar effects were elicited by electrical stimulation of the central trunk of the transected vagus and aortic depressor nerves (vagus-ADN). Transection of the nerves abolished the effect of phenylephrine on the release of noradrenaline in the locus coeruleus. Nerve transections attenuated slightly the decreased release of noradrenaline elicited by phenylephrine in the posterior hypothalamus, while the reduced dopamine release rate was not influenced. The selective stimulation of baroreceptors in the carotid sinus by an inflatable catheter did not influence the release of catecholamines in the locus coeruleus, while release rates of noradrenaline and dopamine in the posterior hypothalamus were decreased. The simultaneous superfusion of locus coeruleus and hypothalamus revealed that, in both areas, noradrenaline release is inhibited by baroreceptor activation. Noradrenergic neurons of the posterior hypothalamus are inhibited by baroreceptor impulses conducted by the carotid sinus nerve and vagus-ADN, while the noradrenergic neurons of the locus coeruleus seem to respond to impulses transmitted by vagus-ADN.(ABSTRACT TRUNCATED AT 250 WORDS)
我们之前已经表明，实验诱导的血压变化会改变下丘脑和蓝斑中儿茶酚胺的释放速率。本研究的目的是确定负责这些脑区儿茶酚胺释放变化的外周压力感受器和向心通路。在麻醉的猫中，将推挽式套管双侧插入蓝斑和下丘脑后部。这两个脑区同时用人造脑脊液进行灌流。苯肾上腺素诱导的血压升高激活压力感受器，降低了蓝斑中去甲肾上腺素的释放速率以及下丘脑后部去甲肾上腺素和多巴胺的释放速率。切断迷走神经和主动脉减压神经的中枢干进行电刺激也产生了类似的效果。神经切断消除了苯肾上腺素对蓝斑中去甲肾上腺素释放的影响。神经切断略微减弱了苯肾上腺素在下丘脑后部引起的去甲肾上腺素释放减少，而多巴胺释放速率的降低则不受影响。通过可充气导管选择性刺激颈动脉窦中的压力感受器，对蓝斑中儿茶酚胺的释放没有影响，而下丘脑后部去甲肾上腺素和多巴胺的释放速率则降低。蓝斑和下丘脑的同时灌流表明，在这两个区域，压力感受器激活均抑制去甲肾上腺素的释放。下丘脑后部的去甲肾上腺素能神经元受到颈动脉窦神经和迷走神经 - 主动脉减压神经传导的压力感受器冲动的抑制，而蓝斑的去甲肾上腺素能神经元似乎对迷走神经 - 主动脉减压神经传递的冲动有反应。（摘要截断于250字）
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