Effect of atrial natriuretic peptide on α-methyl- d-glucoside intestinal active uptake in rats

In vivo, atrial natriuretic peptide (ANP) inhibits water and sodium absorption by the intestine. In addition, ANP inhibits glucose (re)absorption at the level of both the intestine and kidney. ANP also decreases sodium absorption in the rat small intestine in vitro, but only if glucose is present on the luminal side of the tissue. These findings suggest that ANP inhibits the sodium-glucose cotransporter (SGLT) of enterocytes. In the present study the inhibitory effect of 1 μM ANP on SGLT1 in rat small intestine and colon was tested. For this purpose, the apparent kinetic constants of SGLT1 were determined using radioactive α-methyl- d-glucoside (α-MG), a non-metabolizable glucose analogue that selectively serves the luminal Na +-dependent intestinal uptake, but not the serosal-facilitated diffusion sugar carrier. In both tissues, incubation with ANP increased K m without modifying the V max. In addition, V max in the small intestine was found to be higher than in the colon. The evidence presented here suggests that ANP, through its second messenger, may be a competitive inhibitor of SGLT1. Since SGLT1 is also expressed in the brush-border membrane of the renal proximal tubule, we suggest that this peptide might regulate the hydro-saline balance at intestinal and proximal tubular nephron levels.