The sodium-potassium pump in volume expanded hypertension.
The sodium-potassium pump in volume expanded hypertension.
复制标题
钠钾泵体积扩张高血压。
DOI：
10.3109/10641967809068611
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发表时间：
1978
影响因子：
12.3
通讯作者：
D. Clough
中科院分区：
文献类型：
--
作者：
F. Haddy;M. Pamnani;D. Clough
动脉Na+-K+泵和心脏Na+， K-+ atp酶活性降低已经在几种实验性容量扩张型高血压中得到证实。这些变化不是继发于血压升高，因为它们也发生在静脉和右心室，那里的压力没有升高。正常大鼠急性体积扩张可重现动脉Na+-K+泵活性降低，该大鼠血浆提取物应用于另一只大鼠动脉时可抑制泵活性。抑制动脉、静脉和心脏的Na+-K+泵活性，例如用乌巴因，可导致收缩活性增加。因此，容积扩张、泵活性降低和高血压似乎与一种类似瓦阿班的体液剂有因果关系。某些其他证据表明，泵缺陷延伸到交感神经末梢，从而降低了神经代偿机制的效率。
Decreased arterial Na+-K+ pump and cardiac Na+, K-+ATPase activities have now been demonstrated in several types of experimental volume expanded hypertension. The changes are not secondary to elevated pressure since they also occur in veins and right ventricle where the pressure is not elevated. Decreased arterial Na+-K+ pump activity can be reproduced by acute volume expansion of the normal rat and plasma extracts from this rat suppress pump activity when applied to arteries from another rat. Suppression of Na+-K+ pump activity in arteries, veins and heart, with ouabain for example, leads to increased contractile activity. Thus the volume expansion, reduced pump activity, and hypertension appear to be causally related through an ouabain-like humoral agent. Certain other evidence suggests that the pump defect extends to the sympathetic nerve endings, thereby reducing the efficiency of neural compensatory mechanisms.