Abstract
The role of the AT1 receptor in stimulating colonic K+ secretion was investigated in rats with chronic renal failure (CRF) induced by 5/6 nephrectomy. Compared to control rats, CRF rats up-regulate mucosal AT1 receptors approximately two-fold in the proximal (PC) and distal (DC) colonic segments. In contrast, there was no alteration in AT1 receptor protein mass in jejunal or ileal mucosa. Using 86Rb+ as a tracer for transmural K+ fluxes, a significant stimulation of the basal K+ secretory flux across both PC and DC was observed in vitro and this alteration in K+ transport was temporally correlated with the increase in angiotensin II (ANG II) receptors. In both PC and DC the significant increases in the receptor protein were evident 48 h after partial nephrectomy and they were sustained through 6 weeks. These studies support the hypothesis that CRF-induced secretion of K+ is mediated by an up-regulation of AT1 receptors exclusively in the large intestinal segments.
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