WILSON C
Can Med Assoc J. 1964 Oct 31;91(18):964-70.
The possible relationship between the renal mechanism of volume control and blood pressure regulation is discussed. Expansion of the extracellular fluid (ECF) and plasma volumes was demonstrated following renal artery constriction in the rat; after about one month ECF volume returned to normal although hypertension persisted. Measurements of cardiac output in the unanesthetized rat by an implanted electromagnetic flowmeter showed an initial rise in cardiac output after renal artery constriction, returning to normal in 10 to 15 days. A homeostatic hypothesis for the production of renal hypertension is put forward in which changes in ECF volume, capacity vessel tone and myocardial contractility participate in the development of hypertension by elevating cardiac output. Autoregulation of peripheral flow then occurs and the consequent restoration of blood pressure at a renal pressure receptor results in return to normal of cardiac output by negative feedback. Thus in chronic hypertension the high peripheral resistance is maintained by autoregulation.
本文讨论了容量控制的肾脏机制与血压调节之间可能存在的关系。在大鼠肾动脉狭窄后，细胞外液（ECF）和血浆容量出现扩张；大约一个月后，尽管高血压持续存在，但ECF容量恢复正常。通过植入式电磁流量计对未麻醉大鼠的心输出量进行测量，结果显示肾动脉狭窄后心输出量最初会升高，并在10至15天内恢复正常。本文提出了一个关于肾性高血压产生的稳态假说，即ECF容量、容量血管张力和心肌收缩力的变化通过提高心输出量参与高血压的发展。随后发生外周血流的自动调节，肾压力感受器处血压的相应恢复通过负反馈使心输出量恢复正常。因此，在慢性高血压中，高外周阻力通过自动调节得以维持。
