de Wardener H
Nephrologie. 1987;8(1):3-6.
Acute volume expansion, an increase in sodium intake and a restraint on sodium excretion endow the plasma with the capacity to cause a natriuresis, to inhibit sodium transport and to stimulate vascular reactivity. One natriuretic substance, the atrial natriuretic peptide, has been identified. Cytochemical techniques can detect the presence of a Na-K ATPase inhibitor in the plasma of normal man and the rat, the concentration of which is controlled by salt intake. The substance responsible appears to originate in the hypothalamus. The plasma concentration of the cytochemically detectable Na-K ATPase inhibitor is substantially raised in the plasma of patients with essential hypertension, of the spontaneously hypertensive rat and of the Milan hypertensive rat. An hypothesis is put forward that links salt intake, a genetic renal lesion, the endogenous Na-K ATPase inhibitor, the atrial natriuretic peptide, and the substance responsible for vascular reactivity, with the rise in arterial pressure in hereditary forms of hypertension.
急性血容量扩张、钠摄入增加以及钠排泄受限使血浆具有引起利钠作用、抑制钠转运和刺激血管反应性的能力。一种利钠物质，即心钠素，已被识别。细胞化学技术可检测到正常人和大鼠血浆中存在钠钾ATP酶抑制剂，其浓度受盐摄入量控制。相关物质似乎起源于下丘脑。在原发性高血压患者、自发性高血压大鼠和米兰高血压大鼠的血浆中，细胞化学可检测到的钠钾ATP酶抑制剂的血浆浓度显著升高。有人提出一种假说，将盐摄入、遗传性肾损害、内源性钠钾ATP酶抑制剂、心钠素以及负责血管反应性的物质与遗传性高血压形式的动脉压升高联系起来。
