Kurtz Theodore W, DiCarlo Stephen E, Morris R Curtis
Department of Laboratory Medicine, University of California, San Francisco, California, USA.
Department of Physiology, Wayne State University, Detroit, Michigan, USA.
Am J Hypertens. 2016 Dec 1;29(12):1325-1331. doi: 10.1093/ajh/hpw073.
The term "abnormal pressure natriuresis" refers to a subnormal effect of a given level of blood pressure (BP) on sodium excretion. It is widely believed that abnormal pressure natriuresis causes an initial increase in BP to be sustained. We refer to this view as the "pressure natriuresis theory of chronic hypertension." The proponents of the theory contend that all forms of chronic hypertension are sustained by abnormal pressure natriuresis, irrespective of how hypertension is initiated. This theory would appear to follow from "the three laws of long-term arterial pressure regulation" stated by Guyton and Coleman more than 3 decades ago. These "laws" articulate the concept that for a given level of salt intake, the relationship between arterial pressure and sodium excretion determines the chronic level of BP. Here, we review and examine the recent assertion by Beard that these "laws" of long-term BP control amount to nothing more than a series of tautologies. Our analysis supports Beard's assertion, and also indicates that contemporary investigators often use tautological reasoning in support of the pressure natriuresis theory of chronic hypertension. Although the theory itself is not a tautology, it does not appear to be testable because it holds that abnormal pressure natriuresis causes salt-induced hypertension to be sustained through abnormal increases in cardiac output that are too small to be detected.
“压力性钠排泄异常”这一术语指的是特定血压水平对钠排泄的作用低于正常水平。人们普遍认为,压力性钠排泄异常会使血压的初始升高得以持续。我们将这一观点称为“慢性高血压的压力性钠排泄理论”。该理论的支持者认为,所有形式的慢性高血压都是由压力性钠排泄异常维持的,无论高血压是如何引发的。这一理论似乎源于盖顿和科尔曼在30多年前提出的“长期动脉血压调节的三大定律”。这些“定律”阐述了这样一个概念,即对于给定的盐摄入量水平,动脉血压与钠排泄之间的关系决定了血压的慢性水平。在此,我们回顾并审视了比尔德最近提出的断言,即这些长期血压控制的“定律”只不过是一系列同义反复。我们的分析支持了比尔德的断言,同时也表明当代研究人员经常使用同义反复的推理来支持慢性高血压的压力性钠排泄理论。尽管该理论本身并非同义反复,但它似乎无法得到验证,因为它认为压力性钠排泄异常会通过心输出量的异常增加来维持盐诱导的高血压,而这种增加过小以至于无法检测到。