Esler M D
Human Autonomic Function Laboratory, Baker Medical Research Institute, Prahran, Melbourne, Australia.
Baillieres Clin Endocrinol Metab. 1993 Apr;7(2):415-38. doi: 10.1016/s0950-351x(05)80182-x.
Given the ubiquitous distribution of catecholamines in mammals, and their importance in a range of physiological processes pivotal to blood pressure regulation, the subject of catecholamines and essential hypertension has a broader context than simply consideration of sympathetic nervous system and adrenal medullary dysfunction. These further matters are the likely involvement in hypertension pathogenesis of the CNS catecholaminergic neurones influencing peripheral sympathetic outflow, the possible pathogenetic significance of adrenaline released as a cotransmitter in sympathetic nerves, and the natriuretic renal tubular dopamine mechanisms for regulating body sodium balance which appear to be impaired in patients with essential hypertension. The central consideration, however, remains the important issue of the causes and consequences of the now well-documented sympathetic nervous overactivity which characterizes the early developmental phases of essential hypertension.
鉴于儿茶酚胺在哺乳动物体内广泛分布,且它们在一系列对血压调节至关重要的生理过程中具有重要作用,儿茶酚胺与原发性高血压这一主题具有比单纯考虑交感神经系统和肾上腺髓质功能障碍更广泛的背景。这些进一步的问题包括:影响外周交感神经输出的中枢神经系统儿茶酚胺能神经元可能参与高血压发病机制;作为交感神经共递质释放的肾上腺素可能具有的发病学意义;以及调节机体钠平衡的利钠肾小管多巴胺机制,而原发性高血压患者的该机制似乎受损。然而,核心考量仍然是现已充分证实的交感神经活动过度这一重要问题,它是原发性高血压早期发展阶段的特征。