Grisk Olaf, Rettig Rainer
Department of Physiology, Ernst-Moritz-Arndt-University of Greifswald, Greifswalder Str 11c, D-17495 Karlsburg, Germany.
Cardiovasc Res. 2004 Feb 1;61(2):238-46. doi: 10.1016/j.cardiores.2003.11.024.
Elevated sympathetic activity changes renal function and accelerates the development of hypertension. Principles of sympatho-renal interactions in chronic hypertension are reviewed. Alterations in the ontogeny of the sympathetic nervous system and the kidney, inherited abnormalities in sensory receptor function and exaggerated responsiveness to mental stress contribute to inappropriately high sympathetic activity in primary or essential hypertension. Careful characterization of clinical study populations shows that elevated sympathetic activity and "essential" hypertension are not unequivocally associated. Prospective clinical studies which investigate a broader array of physiological functions and experiments in recombinant inbred rodents with less traumatic nerve recording techniques than currently available will help to define under which conditions elevated sympathetic activity is indeed a cause of primary hypertension. Signals arising from the kidney which activate the renin-angiotensin system and afferent renal nerves increase sympathetic activity. These mechanisms importantly contribute to the pathogenesis of hypertension secondary to renal artery stenosis and end-stage renal disease.
交感神经活动增强会改变肾功能并加速高血压的发展。本文综述了慢性高血压中交感神经与肾脏相互作用的原理。交感神经系统和肾脏个体发育的改变、感觉受体功能的遗传异常以及对精神压力的过度反应，都导致原发性或特发性高血压患者交感神经活动异常增高。对临床研究人群的仔细特征分析表明，交感神经活动增强与“原发性”高血压之间并无明确关联。未来的临床研究若能调查更广泛的生理功能，并采用比现有技术创伤性更小的神经记录技术，对重组近交系啮齿动物进行实验，将有助于确定在何种情况下交感神经活动增强确实是原发性高血压的病因。肾脏产生的激活肾素 - 血管紧张素系统和肾传入神经的信号会增加交感神经活动。这些机制在肾动脉狭窄和终末期肾病继发的高血压发病机制中起着重要作用。
