Hall John E
Department of Physiology and Biophysics and Center of Excellence in Cardiovascular-Renal Research, The University of Mississippi Medical Center, Jackson, MS 39216-4505, USA.
Hypertension. 2003 Mar;41(3 Pt 2):625-33. doi: 10.1161/01.HYP.0000052314.95497.78. Epub 2003 Jan 20.
This paper provides a personal perspective of the role of abnormal renal-pressure natriuresis in the pathogenesis of hypertension. Direct support for a major role of renal-pressure natriuresis in long-term control of arterial pressure and sodium balance comes from studies demonstrating that (1) pressure natriuresis is impaired in all forms of chronic hypertension and (2) prevention of pressure natriuresis from operating, by servo-control of renal perfusion pressure, also prevents the maintenance of sodium balance hypertension. Although the precise mechanisms of impaired pressure natriuresis in essential hypertension have remained elusive, recent evidence suggests that obesity and overweight may play a major role. Obesity increases renal sodium reabsorption and impairs pressure natriuresis by activation of the renin-angiotensin and sympathetic nervous systems and by altered intrarenal physical forces. Chronic obesity also causes marked structural changes in the kidneys that eventually lead to a loss of nephron function, further increases in arterial pressure, and severe renal injury in some cases. Although there are many unanswered questions about the mechanisms of obesity hypertension and renal disease, this is one of the most promising areas for future research, especially in view of the growing, worldwide "epidemic" of obesity.
本文从个人角度阐述了异常肾压力性钠排泄在高血压发病机制中的作用。肾压力性钠排泄在动脉血压和钠平衡的长期控制中起主要作用，这一观点得到了以下研究的直接支持：（1）在所有形式的慢性高血压中，压力性钠排泄均受损；（2）通过对肾灌注压的伺服控制来阻止压力性钠排泄的发生，同样也能阻止钠平衡高血压的维持。尽管原发性高血压中压力性钠排泄受损的确切机制仍不清楚，但最近的证据表明，肥胖和超重可能起主要作用。肥胖通过激活肾素 - 血管紧张素和交感神经系统以及改变肾内物理力量，增加肾钠重吸收并损害压力性钠排泄。慢性肥胖还会导致肾脏发生显著的结构变化，最终导致肾单位功能丧失、动脉血压进一步升高，在某些情况下还会导致严重的肾损伤。尽管关于肥胖性高血压和肾脏疾病的机制仍有许多未解决的问题，但鉴于全球范围内肥胖“流行”的加剧，这是未来研究最有前景的领域之一。
