Blaustein M P
Am J Physiol. 1977 May;232(5):C165-73. doi: 10.1152/ajpcell.1977.232.5.C165.
An attempt is made to elucidate the cellular mechanisms which may account for the well-documented correlation between sodium metabolism and peripheral vascular resistance. As a starting point, the evidence that the Na electrochemical gradient across the vascular smooth muscle cell plasma membrane (sarcolemma) plays an important role in cell calcium regulation is reviewed. Because there is significant resting tension ("tone") in most resistance vessels, the ionized Ca2+ level ([Ca2+]1) in the smooth muscle fibers in these vessels must be maintained above the contraction threshold. Consequently, the Ca transport system in the sarcolemma, presumably an Na-Ca exchange mechanism, must be set so as to hold [Ca2+]1 at this suprathreshold level. Any change in the Na gradient will then be reflected as a change in [Ca2+]1 and, therefore, in steady vessel wall tension and peripheral resistance. The correlation between Na metabolism and hypertension could then be accounted for if a circulating agent, perhaps the "natriuretic hormone," affects the Na gradient (across the sarcolemma) and, therefore, [Ca2+]1 and tension.
本文试图阐明细胞机制，这些机制可能解释钠代谢与外周血管阻力之间已被充分证明的相关性。作为起点，本文回顾了如下证据：跨血管平滑肌细胞质膜（肌膜）的钠电化学梯度在细胞钙调节中起重要作用。由于大多数阻力血管存在显著的静息张力（“紧张度”），这些血管平滑肌纤维中的游离钙离子水平（[Ca2+]i）必须维持在收缩阈值以上。因此，肌膜中的钙转运系统，推测为钠-钙交换机制，必须设置为将[Ca2+]i维持在该阈值以上水平。钠梯度的任何变化都将反映为[Ca2+]i的变化，进而反映为血管壁张力和外周阻力的稳定变化。如果一种循环因子，可能是“利钠激素”，影响钠梯度（跨肌膜），进而影响[Ca2+]i和张力，那么钠代谢与高血压之间的相关性就可以得到解释。
