Local upregulation of colonic angiotensin II receptors enhances potassium excretion in chronic renal failure
Local upregulation of colonic angiotensin II receptors enhances potassium excretion in chronic renal failure
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DOI：
10.1152/ajprenal.1998.274.2.f275
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发表时间：
1998-02-01
影响因子：
4.2
通讯作者：
Vaziri, ND
中科院分区：
文献类型：
--
作者：
Hatch, M;Freel, RW;Vaziri, ND
本文观察了血管紧张素Ⅱ（ANG Ⅱ）在慢性肾功能衰竭（CRF）大鼠结肠钾分泌中的作用。通过给大鼠注射AT（1）受体拮抗剂氯沙坦，（86）Rb（+）（作为K（+）的示踪剂）穿过CRF远端结肠的基础净分泌通量（-0.20 +/- 0.04 μ eq.cm（-2）. h（-1））被逆转为吸收通量（0.35 +/- 0.05 μ eq.cm（-2）.h（-1））。当将洛沙坦加入体外CRF结肠组织中时，也观察到类似的结果。相比之下，AT（2）受体拮抗剂PD-123319不能逆转CRF诱导的Rbi通过短路结肠组织转运的改变。CRF大鼠和正常大鼠的血浆ANG II、醛固酮和K（+）浓度以及结肠组织ANG II含量相似。然而，与正常（B（max）= 15.2 +/- 0.4 fmol/mg蛋白）相比，CRF大鼠远端结肠中特异性（125）I标记的ANG II结合位点增加了两倍[最大特异性结合（B（max））= 28.6 +/- 1.6 fmol/mg蛋白]。这些研究表明CRF诱导的结肠K（+）分泌是通过CRF中AT（1）受体的上调介导的。
The role of angiotensin II (ANG II) in colonic secretion of K(+) was examined in rats with chronic renal failure (CRF). The basal net secretory flux of (86)Rb(+) (as a tracer for K(+)) across the CRF distal colon (-0.20 +/- 0.04 mu eq.cm(-2).h(-1)) was reversed to an absorptive flux (0.35 +/- 0.05 mu eq.cm(-2).h(-1)) by injecting the rats with the AT(1) receptor antagonist, losartan. it similar result was observed when losartan was added to the CRF colonic tissue in vitro. In contrast, an AT(2) receptor antagonist, PD-123319, did not reverse the CRF-induced alterations in Rbi transport across the short-circuited colonic tissue. Plasma concentrations of ANG II, aldosterone, and K(+), as well as the ANG II content of colonic tissues from CRF and normal rats, were similar. However, specific (125)I-labeled ANG II binding sites in rat distal colon increased twofold in CRF [maximal specific binding (B(max)) = 28.6 +/- 1.6 fmol/mg protein] compared with normal (B(max) = 15.2 +/- 0.4 fmol/mg protein). These studies suggest that CRF-induced secretion of K(+) by the colon is mediated by an upregulation of AT(1) receptors present in CRF.