Haddy F J, Pamnani M B
Department of Physiology, Uniformed Services University, Bethesda, MD 20814, USA.
Clin Exp Hypertens. 1998 Jul-Aug;20(5-6):499-508. doi: 10.3109/10641969809053228.
Three lines of evidence led to our suggestion in 1976 that sodium pump inhibitors are involved in volume expanded hypertension. These were 1) pressor activity of low renin hypertensive blood 2) natriuretic and sodium pump inhibiting activities of volume expanded blood and 3) potassium vasoactivity which was blocked by ouabain and suppressed potassium vasodilatation, myocardial Na-K-ATPase, and artery, vein and WBC sodium pumps in low renin hypertension. This led to bioassay of plasma from acutely volume expanded dogs and from dogs with one-kidney, one wrapped hypertension for sodium pump inhibiting activity that acts on arteries. Positive results were reported in 1980. The assay was also positive in rats with one-kidney, one clip and reduced renal mass hypertension (but not in rats with spontaneous or salt sensitive hypertension) and in humans with acute volume expansion and low renin essential hypertension (but not in humans with normal renin hypertension). Thus the inhibitor which acts on the sodium pump in arteries appears to be present only in low renin hypertension.
1976年，三条证据线索促使我们提出钠泵抑制剂与容量扩张性高血压有关的观点。这些证据是：1）低肾素高血压血液的升压活性；2）容量扩张血液的利钠和钠泵抑制活性；3）钾血管活性，它被哇巴因阻断，并在低肾素高血压中抑制钾血管舒张、心肌钠钾ATP酶以及动脉、静脉和白细胞钠泵。这导致了对急性容量扩张犬和一侧肾、一侧肾被包裹性高血压犬的血浆进行生物测定，以检测作用于动脉的钠泵抑制活性。1980年报告了阳性结果。该测定在一侧肾、一侧夹闭并肾质量减少性高血压大鼠（但自发性或盐敏感性高血压大鼠中未出现）以及急性容量扩张和低肾素原发性高血压患者（但正常肾素高血压患者中未出现）中也呈阳性。因此，作用于动脉钠泵的抑制剂似乎仅存在于低肾素高血压中。
