Elghozi J L, Miach P, Meyer P
Nouv Presse Med. 1978 Mar 4;7(3):743-4, 749-51.
Several models of experimental hypertension are described (neurogenic, mineralocorticoid, renovascular and genetic hypertension). An activation of the sympathetic nervous system is seen in these situations (increases in sympathetic nervous discharge, in the synthesis of noradrenaline and in the level of plasma catecholamines). This activation may be connected with biochemical abnormalities within the medulla which have been noticed for catecholamines and serotonin. These medullary abnormalities could themselves depend on abnormalities situated at higher levels (hypothalamus). The factors which determine the central problem and their mechanism of action are still hypothetical (e.g. the direct effect of sodium on the brain, the effect of stress and the environment as well as genetically determined biochemical abnormalities of the central nervous system). In the case of essential hypertension in man, available data are limited to the levels of plasma catecholamines which suggest an increased sympathetic activity of central origin when these levels are elevated.
本文描述了几种实验性高血压模型(神经源性、盐皮质激素性、肾血管性和遗传性高血压)。在这些情况下可观察到交感神经系统的激活(交感神经放电增加、去甲肾上腺素合成增加以及血浆儿茶酚胺水平升高)。这种激活可能与髓质内儿茶酚胺和5-羟色胺的生化异常有关。这些髓质异常本身可能取决于更高水平(下丘脑)的异常。决定核心问题的因素及其作用机制仍属推测(例如钠对大脑的直接作用、应激和环境的影响以及中枢神经系统的遗传决定生化异常)。对于人类原发性高血压,现有数据仅限于血浆儿茶酚胺水平,当这些水平升高时提示中枢起源的交感神经活动增加。