肾小球后血管收缩到血管紧张素II和去甲肾上腺素依赖于细胞内钙的释放

John D. Imig, Anthony K. Cook, Edward W. Inscho
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引用次数: 18

摘要

本研究旨在确定环吡唑酸(CPA)对肾小球前和肾小球后血管收缩剂对血管紧张素II (ANG II)和去甲肾上腺素(NE)的反应的影响。CPA治疗显著降低了传入小动脉对10 nM ANG II的反应51%,对1000 nM NE的反应19%。在CPA的存在下,对ANG II和NE的传出小动脉反应也大大减弱。这些数据表明,传入和传出小动脉对ANG II和NE的反应依赖于钙从对cpa敏感的细胞内储存的释放。此外,对这些药物的肾小球后反应更依赖于细胞内储存的钙释放。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Postglomerular vasoconstriction to angiotensin II and norepinephrine depends on intracellular calcium release

The current study was performed to determine the effect of calcium store depletion with cyclopiazonic acid (CPA) on the pre- and postglomerular vasoconstrictor responses to angiotensin II (ANG II) and norepinephrine (NE). CPA treatment significantly attenuated the afferent arteriolar response to 10 nM ANG II by 51% and to 1000 nM NE by 19%. Efferent arteriolar responses to ANG II and NE were also greatly attenuated in the presence of CPA. These data demonstrate that afferent and efferent arteriolar responses to ANG II and NE depend on release of calcium from CPA-sensitive intracellular stores. Furthermore, the postglomerular response to these agents exhibits a greater dependency on calcium release from intracellular stores.

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