Role of chloride in constriction of descending vasa recta by angiotensin II.

Role of chloride in constriction of descending vasa recta by angiotensin II.
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氯化物在血管紧张素 II 导致的直降血管收缩中的作用。

DOI:
10.1152/ajpregu.2001.280.6.r1878
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发表时间:
2001
期刊:
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子:
--
通讯作者:
Pallone,TL
Pallone,TL
中科院分区:
--
文献类型:
--
作者:
Zhang,Z;Huang,JM;Turner,MR;Rhinehart,KL;Pallone,TL

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我们研究了血管紧张素II(10− 8 M)诱导的外髓降直血管(OMDVR)收缩对膜电位(μ m)和氯离子的依赖性。ANG II使OMDVR去极化,如通过用电压敏感性染料双[1,3-二丁基巴比妥酸-(5)]三甲新氧烯醇[DiBAC 4(3)]完全装载它们或选择性装载它们的周细胞所测量的。当用短杆菌肽D穿孔贴片测量时,还观察到ANG II将周细胞从静息值−55.6 ± 2.6 mV降低到−26.2 ± 5.4 mV。当在未受刺激的血管中使用DiBAC 4(3)进行测量时,改变细胞外Cl−浓度([Cl−])或暴露于氯离子通道阻断剂茚满基氧基乙酸94(IAA-94; 30 μM)都不会影响Δ μ m。相反,IAA-94复极化OMDVR与ANG Ⅱ。IAA-94(30 μM)和尼氟灭酸(30 μM,1 mM)均不影响未受刺激的OMDVR的血管活性,而两者均扩张ANG II预收缩的血管。细胞外[Cl−]从150 meq/l减少到30 meq/l增强ANG II诱导的收缩。最后,我们确定了OMDVR周细胞中的Cl−通道,该通道由ANG II或切除到细胞外缓冲液中激活。我们的结论是血管紧张素II收缩OMDVR涉及周细胞去极化,部分原因是氯离子通道活性增加。
We investigated the dependence of ANG II (10−8M)-induced constriction of outer medullary descending vasa recta (OMDVR) on membrane potential (Ψm) and chloride ion. ANG II depolarized OMDVR, as measured by fully loading them with the voltage-sensitive dye bis[1,3-dibutylbarbituric acid-(5)] trimethineoxonol [DiBAC4(3)] or selectively loading their pericytes. ANG II was also observed to depolarize pericytes from a resting value of −55.6 ± 2.6 to −26.2 ± 5.4 mV when measured with gramicidin D-perforated patches. When measured with DiBAC4(3) in unstimulated vessels, neither changing extracellular Cl−concentration ([Cl−]) nor exposure to the chloride channel blocker indanyloxyacetic acid 94 (IAA-94; 30 μM) affected Ψm. In contrast, IAA-94 repolarized OMDVR pretreated with ANG II. Neither IAA-94 (30 μM) nor niflumic acid (30 μM, 1 mM) affected the vasoactivity of unstimulated OMDVR, whereas both dilated ANG II-preconstricted vessels. Reduction of extracellular [Cl−] from 150 to 30 meq/l enhanced ANG II-induced constriction. Finally, we identified a Cl−channel in OMDVR pericytes that is activated by ANG II or by excision into extracellular buffer. We conclude that constriction of OMDVR by ANG II involves pericyte depolarization due, in part, to increased activity of chloride channels.
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