THE SYMPATHETIC SYSTEM IN HYPERTENSION - STATE-OF-THE-ART REVIEW
THE SYMPATHETIC SYSTEM IN HYPERTENSION - STATE-OF-THE-ART REVIEW
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DOI：
10.1161/01.hyp.4.3_pt_2.208
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发表时间：
1982-01-01
期刊：
影响因子：
8.3
通讯作者：
ABBOUD, FM
中科院分区：
文献类型：
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作者：
ABBOUD, FM
人们可以假设细胞膜渗透性、钠转运或血管肌钠泵的遗传缺陷，这可以解释细胞内钠增加和血管收缩性增强的原因。如果电致钠泵过度活跃，如SHR，其抑制可能导致显著的去极化和更大的收缩。交感神经支配可能对膜异常的发展以及肥厚性血管变化的发展至关重要，两者都增强了收缩和血管张力。动脉拉伸受体感觉末端的类似膜缺陷可能是高血压早期或某些遗传模型中高血压发病前出现的动脉压力感受器反射受损的原因。这种缺陷可能与受体区域的钠泵或钠运输有关，导致压力感受器放电减少和压力感受器的应变敏感性降低，导致交感驱动的夸大。我们还需要进一步的信息来了解高血压中各种传入神经的压力反射控制。肾上腺素能神经末梢的另一种膜缺陷可能促进内源性NE的释放。过量的盐摄入可能会暴露或夸大膜缺陷。在中枢神经系统中，谷氨酰胺、NE或GABA受体的缺陷可能导致高中枢交感驱力。受体对各种压力神经肽（如血管紧张素和亮氨酸脑啡肽）的更大亲和力或这些肽的更大释放也可能是中枢神经系统交感神经过度激活或中枢水平压力反射损伤的原因。在高血压的不同阶段，心脏受体可能对交感驱动有不同的影响，这取决于心脏肥厚的程度或心脏的大小。最后，肾传入神经活动的增加可能引起交感神经活动的增加，并在高血压患者的利钠因子和交感神经系统之间提供联系。
One may postulate a genetic defect in membrane permeability, in the transport of sodium, or in the sodium pump in vascular muscle which could account for increased intracellular sodium and enhanced vascular contractility. If the electrogenic sodium pump is overactive, as in SHR, its inhibition may lead to significant depolarization and greater contraction. Sympathetic innervation may be essential for the development of membrane abnormality as well as for the development of hypertrophic vascular changes, both of which augment contraction and vascular tone. A similar membrane defect at the sensory endings of arterial stretch receptors may account for impaired arterial baroreceptor reflexes seen in very early phases of hypertension or, in some genetic models, before hypertension develops. This defect may be related to the sodium pump or sodium transport in the receptor region and cause a decrease in baroreceptor discharge and in the strain-sensitivity of the baroreceptors, resulting in exaggerated sympathetic drive. Further information is needed on the baroreflex control of various efferents in hypertension. Another membrane defect at the adrenergic nerve terminals may facilitate release of endogenous NE. Excessive salt intake may unmask or exaggerate the membrane defects. In the central nervous system a defect in glutamine, NE, or GABA receptors may contribute to a high central sympathetic drive. Greater receptor affinity to various pressor neuropeptides such as angiotensin and leucine enkephalin or greater release of these peptides may also account for the excessive CNS sympathetic activation or impairment of baroreflexes at a central level. Cardiac receptors may have a variable influence on sympathetic drive in the various stages of hypertension, depending on the degree of cardiac hypertrophy or cardiac size. Finally, increased renal afferent nerve activity may provoke an increase in sympathetic activity and provide a link between natriuretic factors and the sympathetic nervous system in hypertension.