Guyton A C
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216.
Am J Physiol. 1990 Nov;259(5 Pt 2):R865-77. doi: 10.1152/ajpregu.1990.259.5.R865.
Long-term arterial pressure control is very different from acute control, because many of the acute control systems are overridden by a single long-term mechanism that has little to do with short-term control. This is the renal fluid volume mechanism for pressure control. It is based on a simple functional property of the kidney: as the arterial pressure rises, the kidney output of water and electrolytes increases dramatically. When the output rises above the net intake of water and electrolytes, negative body fluid balance occurs, causing both the body fluid volume and the pressure to decrease. This decrease continues until the kidney fluid output exactly balances the net fluid intake. Conversely, if the pressure falls below the exact level for balance, intake becomes greater than output; then fluid builds up in the body and the pressure rises until intake and output again exactly balance each other. This fluid mechanism for pressure control has been known from the beginning of blood pressure research. However, its overpowering importance was not appreciated until a mathematical computer analysis in 1966 demonstrated the renal-fluid feedback mechanism to have infinite feedback gain for long-term pressure control. This is the principal topic of the present review.
长期动脉血压控制与急性控制有很大不同,因为许多急性控制系统被一种与短期控制几乎无关的单一长期机制所取代。这就是肾脏体液容量压力控制机制。它基于肾脏的一个简单功能特性:随着动脉血压升高,肾脏的水和电解质排出量会急剧增加。当排出量超过水和电解质的净摄入量时,机体出现负水平衡,导致体液容量和血压下降。这种下降会持续到肾脏的液体排出量与净液体摄入量完全平衡。相反,如果血压降至平衡所需的精确水平以下,摄入量就会大于排出量;然后体液在体内积聚,血压升高,直到摄入量和排出量再次完全平衡。这种压力控制的体液机制从血压研究一开始就为人所知。然而,直到1966年的一项数学计算机分析证明肾脏体液反馈机制在长期血压控制中具有无限反馈增益,其压倒性的重要性才得到认可。这是本综述的主要主题。