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Local upregulation of colonic angiotensin II receptors enhances potassium excretion in chronic renal failure.

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 of86Rb+(as a tracer for K+) across the CRF distal colon (-0.20 ± 0.04 μeq ⋅ cm-2 ⋅ h-1) was reversed to an absorptive flux (0.35 ± 0.05 μeq ⋅ cm-2 ⋅ h-1) by injecting the rats with the AT1receptor antagonist, losartan. A similar result was observed when losartan was added to the CRF colonic tissue in vitro. In contrast, an AT2 receptor antagonist, PD-123319, did not reverse the CRF-induced alterations in Rb+ 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, specific125I-labeled ANG II binding sites in rat distal colon increased twofold in CRF [maximal specific binding (Bmax) = 28.6 ± 1.6 fmol/mg protein] compared with normal (Bmax = 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 AT1 receptors present in CRF.