NaCl consumption is attenuated in female KCNE1 null mutant mice

The role of potassium channels in the regulation of NaCl intake has not bee n investigated previously. One potassium channel, KCNQ1, and its regulator, KCNE1, are expressed in salivary glands and kidneys, and KCNE1 null mutant mice are deficient in KCNQ1 potassium currents. To understand the role of the KCNQ1/KCNE1 channel complex in NaCl taste and intake, we compared the N aCl consumption of KCNE1 +/+ (129/Sv), KCNE1 +/-, and KCNE1 -/- mice using two-bottle intake tests and lick rate tests. Although KCNE1 +/+ and KCNE1 /- mice exhibited consumption patterns for 75-150 mM NaCl solutions conside red typical for 129/Sv mice, the KCNE1 -/- null mutant 129/Sv mice were ind ifferent to or rejected them. This effect was observed in female mice only, required prior exposure to NaCl solutions, and the extent of rejection was greater after prior exposure to 150 mM NaCl solution than 75 mM NaCl solut ion. No differences were observed in the avidity for KCI solutions or in li ck rates of naive mice for 150 or 300 mM NaCl solutions. These results demo nstrate that a single potassium channel gene can influence voluntary NaCl i ntake. We speculate that disruption of the KCNE1 gene impairs sodium metabo lism in female mice drinking high levels of 150 mM NaCl, which causes malai se that becomes associated with NaCl taste, and as a consequence, reduced p reference for NaCl. (C) 2001 Elsevier Science Inc. All rights reserved.