Haeusler G
Circ Res. 1975 Jun;36(6 Suppl 1):223-32. doi: 10.1161/01.res.36.6.223.
Electrical stimulation of the posterior hypothalamus is followed by an immediate increase in sympathetic nerve activity and rise in blood pressure. Destruction of hypothalamic adrenergic structures by local unilateral injection of 6-hydroxydopamine into the posterior hypothalamus reduced the blood pressure rise in response to stimulation of the lesioned side. This and numerous other findings indicate an involvement of central adrenergic neurons in the mediation of an increase of sympathetic nerve activity caused by hypothalamic stimulation. However, central adrenergic neurons do not seem to be an integral part of the sympathoexcitatory pathways originating in the posterior hypothalamus but rather facilitate their activation: after almost complete norepinephrine depletion produced by combined treatment with reserpine and alpha-methl-p-tyrosine, hypothalamic stimulation was still followed by an increase in spontaneous sympathetic nerve activity. Stimulation of an alpha-adrenoceptive site, probably located in the lower brain stem, mimics an activation of the baroreceptor reflex. The hypotensive drug, clonidine, stimulates this alpha-adrenoceptive site. In low doses clonidine facilitates the activation of the reflex, and in high doses this drug induces a state which closely resembles a pronounced activation of the reflex. Experiments following depletion of norepinephrine suggest that the central part of the baroreceptor reflex arc does not contain adrenergic neurons. However, these findings are compatible with the view that some neurons within the reflex arc are supplied with alpha-adrenoceptors. For the present it cannot be stated with certainty whether these alpha-adrenoceptors possess an innervation by adrenergic neurons projecting onto the reflex arc. In favor of such an innervation are the obsevations that alpha-methyldopa has its site of action in the lower brain stem and that the integrity of central adrenergic neurons is essential for its hypotensive effect. It seems that two central adrenergic systems exist with opposing effects on cardiovascular control. These are an excitatory hypothalamic and an inhibitory bulbar adrenergic system. Partial destruction of central adrenergic neurons by intraventricularly injected 6-hydroxydopamine prevents the development of DOCA/NaCl, renal, and neurogenic hypertension and alters the pattern of blood pressure rise in spontaneously hypertensive rats. Impairment of central adrenergic function or imbalance of the two central adrenergic mechanisms may represent a trigger mechanism for the initiation of hypertension.
刺激下丘脑后部后，交感神经活动立即增强，血压升高。通过向后下丘脑局部单侧注射6-羟基多巴胺破坏下丘脑肾上腺素能结构，可降低对损伤侧刺激的血压升高反应。这一发现以及众多其他研究结果表明，中枢肾上腺素能神经元参与介导下丘脑刺激引起的交感神经活动增强。然而，中枢肾上腺素能神经元似乎并非起源于下丘脑后部的交感兴奋通路的组成部分，而是促进其激活：在用利血平和α-甲基-对酪氨酸联合治疗导致几乎完全去甲肾上腺素耗竭后，刺激下丘脑仍会伴随自发性交感神经活动增强。刺激一个可能位于脑干下部的α-肾上腺素能位点，可模拟压力感受器反射的激活。降压药可乐定可刺激该α-肾上腺素能位点。小剂量可乐定促进反射的激活，大剂量时该药物会诱发一种状态，与反射的明显激活非常相似。去甲肾上腺素耗竭后的实验表明，压力感受器反射弧的中枢部分不包含肾上腺素能神经元。然而，这些发现与反射弧内一些神经元配备有α-肾上腺素能受体的观点相符。目前尚不能确定这些α-肾上腺素能受体是否接受投射到反射弧上的肾上腺素能神经元的支配。支持这种支配的观察结果是，α-甲基多巴的作用部位在脑干下部，且中枢肾上腺素能神经元完整对其降压作用至关重要。似乎存在两个对心血管控制具有相反作用的中枢肾上腺素能系统。这两个系统分别是兴奋性的下丘脑肾上腺素能系统和抑制性的延髓肾上腺素能系统。脑室内注射6-羟基多巴胺对中枢肾上腺素能神经元的部分破坏可预防DOCA/NaCl、肾性和神经源性高血压的发展，并改变自发性高血压大鼠的血压升高模式。中枢肾上腺素能功能受损或两个中枢肾上腺素能机制失衡可能是引发高血压的触发机制。
