Osborn J L
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
Hypertension. 1991 Jan;17(1 Suppl):I91-6. doi: 10.1161/01.hyp.17.1_suppl.i91.
The long-term regulation of arterial pressure requires the maintenance of a balance between sodium and water intake and sodium and water excretion. Normal salt and water balance leads to stable body fluid volumes and the maintenance of normal renal function is critical to establishing extracellular fluid volume homeostasis. This review focuses on the role of the kidney in the long-term control of salt and water balance with particular emphasis on the relations between sodium intake, the renin-angiotensin-aldosterone system, renal sympathetic nerve activity, and the regulation of arterial pressure via renal sodium and water excretion. The accumulation of evidence in recent years demonstrates that low level elevation of renin release, circulating angiotensin II or aldosterone, or activation of renal sympathetic outflow may alter renal function such that normal natriuretic and diuretic responses to arterial pressure are significantly impeded. Under these circumstances, the maintenance of normal sodium and water excretion requires a significant elevation of arterial pressure. Thus, compromised renal function leads to elevation of arterial pressure to maintain adequate sodium and water balance during periods of increased sodium intake. The resultant chronic elevation of arterial pressure then becomes a compromise that is used by the kidneys to maintain normal extracellular body fluid volumes.
动脉血压的长期调节需要维持钠和水的摄入与钠和水的排泄之间的平衡。正常的盐和水平衡导致稳定的体液量，而维持正常的肾功能对于建立细胞外液容量稳态至关重要。本综述重点关注肾脏在盐和水平衡长期控制中的作用，特别强调钠摄入、肾素 - 血管紧张素 - 醛固酮系统、肾交感神经活动以及通过肾钠和水排泄对动脉血压调节之间的关系。近年来积累的证据表明，肾素释放、循环中的血管紧张素 II 或醛固酮的低水平升高，或肾交感神经传出冲动的激活，可能会改变肾功能，从而显著阻碍对动脉血压正常的利钠和利尿反应。在这些情况下，维持正常的钠和水排泄需要显著升高动脉血压。因此，肾功能受损会导致动脉血压升高，以便在钠摄入增加期间维持足够的钠和水平衡。由此导致的动脉血压慢性升高随后成为肾脏用来维持正常细胞外体液量的一种折衷方式。
