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儿茶酚胺对大鼠髓质厚升支氯转运的影响:与血管紧张素 II 的相互作用。

Effect of catecholamines on rat medullary thick ascending limb chloride transport: interaction with angiotensin II.

机构信息

Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9063, USA.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2010 Apr;298(4):R954-8. doi: 10.1152/ajpregu.00758.2009. Epub 2010 Feb 10.

Abstract

Previous studies have shown that in proximal and distal tubule nephron segments, peritubular ANG II stimulates sodium chloride transport. However, ANG II inhibits chloride transport in the medullary thick ascending limb (mTAL). Because ANG II and catecholamines are both stimulated by a decrease in extracellular fluid volume, the purpose of this study was to examine whether there was an interaction between ANG II and catecholamines to mitigate the inhibition in chloride transport by ANG II. In isolated perfused rat mTAL, 10(-8) M bath ANG II inhibited transport (from a basal transport rate of 165.6 +/- 58.8 to 58.8 +/- 29.4 pmol.mm(-1).min(-1); P < 0.01). Bath norepinephrine stimulated chloride transport (from a basal transport rate of 298.1 +/- 31.7 to 425.2 +/- 45.8 pmol.mm(-1).min(-1); P < 0.05) and completely prevented the inhibition in chloride transport by ANG II. The stimulation of chloride transport by norepinephrine was mediated entirely by its beta-adrenergic effect; however, both the beta- and alpha-adrenergic agonists isoproterenol and phenylephrine prevent the ANG II-mediated inhibition in chloride transport. In the presence of 10(-5) M propranolol, the effect of norepinephrine to prevent the inhibition of chloride transport by ANG II was still present. These data are consistent with an interaction of both alpha- and beta-catecholamines and ANG II on net chloride transport in the mTAL.

摘要

先前的研究表明,在近端和远端肾小管肾单位中,管周 ANG II 刺激氯化钠转运。然而,ANG II 抑制髓质升支粗段(mTAL)中的氯离子转运。由于 ANG II 和儿茶酚胺都受到细胞外液体积减少的刺激,本研究的目的是检查 ANG II 和儿茶酚胺之间是否存在相互作用,以减轻 ANG II 对氯离子转运的抑制作用。在分离灌注的大鼠 mTAL 中,10(-8) M 浴 ANG II 抑制转运(从基础转运速率 165.6 +/- 58.8 到 58.8 +/- 29.4 pmol.mm(-1).min(-1);P < 0.01)。浴内去甲肾上腺素刺激氯离子转运(从基础转运速率 298.1 +/- 31.7 到 425.2 +/- 45.8 pmol.mm(-1).min(-1);P < 0.05),并完全阻止 ANG II 对氯离子转运的抑制。去甲肾上腺素对氯离子转运的刺激完全是通过其β-肾上腺素能作用介导的;然而,β-和α-肾上腺素能激动剂异丙肾上腺素和苯肾上腺素均可防止 ANG II 介导的氯离子转运抑制。在存在 10(-5) M 普萘洛尔的情况下,去甲肾上腺素预防 ANG II 抑制氯离子转运的作用仍然存在。这些数据与 mTAL 中 net 氯离子转运中 α-和β-儿茶酚胺和 ANG II 的相互作用一致。

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