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血管加压素诱导大鼠基底动脉产生节律性活动。

Vasopressin induced rhythmic activity in rat basilar artery.

作者信息

Rusch N J, Hermsmeyer K

出版信息

Ann Biomed Eng. 1985;13(3-4):295-302. doi: 10.1007/BF02584247.

Abstract

The effects of vasopressin on membrane potential and tension were studied in isolated segments of basilar arteries from the University of Iowa colonies of normotensive inbred Kyoto-Wistar rats (WKY) and stroke-prone spontaneously hypertensive rats (SP-SHR). In the presence of vasopressin (0.01-0.3 IU/ml), basilar arteries from WKY, but not from SP-SHR, developed rhythmic contractions. These contractions were recorded in 13 of 14 WKY basilar arteries, were unaffected by pretreatment with 6-hydroxydopamine, and were characterized by 20-100 dyne oscillations in tension, occurring 1-3 cycles/min, and superimposed on the vasopressin-induced contraction (averaging 60 dynes at 0.01 IU/ml or 160 dynes at 0.3 IU/ml). However, resting membrane potentials were not different in SP-SHR vs. WKY at 37 degrees C, and both strains showed about the same (11 mV) depolarization by 0.1 IU/ml of vasopressin. The rhythmic contractions were enhanced by K+-free solution, and abolished in the presence of high K+ solution (30 mM), suggesting that active Na+-K+ transport may be involved in modulating the rhythmic activity. These findings are consistent with the hypothesis that the vasopressin-induced rhythmic contractions in WKY basilar arteries are at least partly dependent on a reduced activity of electrogenic Na+-K+ active transport in WKY as compared to SP-SHR.

摘要

在来自爱荷华大学的正常血压近交京都-威斯塔大鼠(WKY)和易中风自发性高血压大鼠(SP-SHR)群体的基底动脉离体节段中,研究了血管加压素对膜电位和张力的影响。在血管加压素(0.01 - 0.3 IU/ml)存在的情况下,WKY的基底动脉会出现节律性收缩,而SP-SHR的基底动脉则不会。在14条WKY基底动脉中的13条记录到了这些收缩,6-羟基多巴胺预处理对其无影响,其特征为张力出现20 - 100达因的振荡,每分钟发生1 - 3个周期,并叠加在血管加压素诱导的收缩上(在0.01 IU/ml时平均为60达因,在0.3 IU/ml时为160达因)。然而,在37℃时,SP-SHR与WKY的静息膜电位并无差异,并且两种品系在0.1 IU/ml血管加压素作用下均表现出约相同程度(11 mV)的去极化。无钾溶液可增强节律性收缩,而在高钾溶液(30 mM)存在时则消失,这表明主动钠钾转运可能参与调节节律性活动。这些发现与以下假设一致,即与SP-SHR相比,WKY基底动脉中血管加压素诱导的节律性收缩至少部分依赖于WKY中电生性钠钾主动转运活性的降低。

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