Campese Vito M, Ku Elaine, Park Jeanie
Division of Nephrology, USC/Keck School of Medicine, University of Southern California, 2020 Zonal Aveue, Los Angeles, CA 90033, USA.
Int J Hypertens. 2011 Jan 20;2011:814354. doi: 10.4061/2011/814354.
Hypertension in chronic renal disease and renovascular disease is often resistant to therapy. Understanding the pathogenic mechanisms responsible for hypertension in these conditions may lead to improved and more targeted therapeutic interventions. Several factors have been implicated in the pathogenesis of hypertension associated with renal disease and/or renal failure. Although the role of sodium retention, total body volume expansion, and hyperactivity of the renin-angiotensin-aldosterone system (RAAS) are well recognized, increasing evidence suggests that afferent impulses from the injured kidney may increase sympathetic nervous system activity in areas of the brain involved in noradrenergic regulation of blood pressure and contribute to the development and maintenance of hypertension associated with kidney disease. Recognition of this important pathogenic factor suggests that antiadrenergic drugs should be an essential component to the management of hypertension in patients with kidney disease, particularly those who are resistant to other modalities of therapy.
慢性肾病和肾血管疾病中的高血压通常对治疗有抵抗性。了解这些情况下导致高血压的致病机制可能会带来改进且更具针对性的治疗干预措施。几个因素与肾病和/或肾衰竭相关的高血压发病机制有关。尽管钠潴留、总体液量增加以及肾素-血管紧张素-醛固酮系统(RAAS)的活性亢进的作用已得到充分认识,但越来越多的证据表明,来自受损肾脏的传入冲动可能会增加大脑中参与去甲肾上腺素能血压调节区域的交感神经系统活动,并促成与肾病相关的高血压的发生和维持。认识到这一重要致病因素表明,抗肾上腺素能药物应成为肾病患者高血压管理的重要组成部分,尤其是那些对其他治疗方式有抵抗性的患者。