Portal hypertension induces sodium channel expression in colonocytes from the distal colon of the rat

Cellular mechanisms for Na+ retention in portal hypertension are undefined, but epithelial Na+ channels (ENaC) may be involved. Under high-salt diet, ENaC are absent from distal colon of rat but can be induced by mineralocort icoids such as aldosterone. Presence of rat ENaC was determined by amilorid e inhibition of Na-22(+) uptake in surface colonocytes 7 and 14 days after partial portal vein ligation (PVL) or sham surgery. At both times, uptake i nhibition was significantly increased in PVL rats. Presence of mRNA transcr ipts, determined by RT-PCR, demonstrated that channel alpha- and gamma -sub units were similarly expressed in both groups but that beta -subunit mRNA w as increased in PVL rats. This confirms that there was induction of rat ENa C and indicates that beta -subunit has a regulatory role. Urinary Na+ was d ecreased for 3 days after PVL but was not different at other times, and ser um aldosterone levels were elevated at 7 days, at a time when urinary Na+ o utput was similar to that of sham-operated rats. We conclude that PVL leads to induction of ENaC in rat distal colon. An increase in aldosterone level s may prevent natiuresis and is probably one of several control mechanisms involved in Na+ retention in portal hypertension.