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主动脉中钠钾ATP酶活性增强可能解释糖尿病患者对氯化钾的收缩反应未改变的原因。

Enhanced Na-K ATPase activity in the aorta may explain the unaltered contractile responses to KCl in diabetes mellitus.

作者信息

Orie N N, Aloamaka C P, Antai A B

机构信息

Department of Physiology, College of Medicine, University of Benin, Nigeria.

出版信息

Indian J Physiol Pharmacol. 1993 Jul;37(3):199-203.

PMID:8276495
Abstract

Sodium-potassium ATPase activity and transmembrane calcium influx in the aortic smooth muscle from control and diabetic rats were assessed indirectly through the measurement of KCl relaxation and contractile responses to CaCl2 in attempts to explain the contractile responses to KCl following streptozotocin-induced diabetes mellitus. There were no significant changes in the maximum contractile responses of the aortas from 4 and 12 week diabetic rats to KCl even when significant increases in calcium influx were demonstratable. On the other hand, the diabetic aortas were significantly (P < 0.05) more sensitive to KCl-induced relaxations than the controls. This provides an indirect evidence for increased activity of the sodium-postassium ATPase enzyme in the aortas from streptozotocin diabetic rats. This may, atleast in part, explain the inability of KCl to produce greater than normal contractions of the aortas from diabetic rats.

摘要

通过测量氯化钾松弛和对氯化钙的收缩反应,间接评估正常大鼠和糖尿病大鼠主动脉平滑肌中的钠钾ATP酶活性和跨膜钙内流,以解释链脲佐菌素诱导的糖尿病后对氯化钾的收缩反应。即使可证明钙内流显著增加,4周和12周糖尿病大鼠主动脉对氯化钾的最大收缩反应也无显著变化。另一方面,糖尿病主动脉对氯化钾诱导的松弛比对照组更敏感(P<0.05)。这为链脲佐菌素糖尿病大鼠主动脉中钠钾ATP酶活性增加提供了间接证据。这至少可以部分解释氯化钾不能使糖尿病大鼠主动脉产生大于正常收缩的原因。

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