de Wardener H E, MacGregor G A
Medicine (Baltimore). 1983 Sep;62(5):310-26. doi: 10.1097/00005792-198309000-00004.
It is proposed that in essential hypertension the underlying genetic lesion is a renal difficulty in excreting sodium, which becomes more apparent the higher the sodium intake. It is further proposed that the renal lesion is the cause of the observed rise in the plasma's capacity to inhibit Na+-K+-ATPase and that the inhibitor's action on vascular smooth muscle eventually leads to the rise in blood pressure.
有人提出，在原发性高血压中，潜在的遗传病变是肾脏排泄钠的功能出现障碍，钠摄入量越高，这种障碍就越明显。进一步提出，肾脏病变是观察到的血浆抑制钠钾ATP酶能力升高的原因，并且该抑制剂对血管平滑肌的作用最终导致血压升高。
