NaCl appetite in two strains of rat reported to be resistant to mineralocorticoid-induced hypertension.

Both Long-Evans (LE) and Wistar-Furth (WF) strains of rat are known to be resistant to development of hypertension by mineralocorticoid (MC) treatment. MC-induced hypertension is, in part, mediated by the brain. We have examined another aspect of central MC action, the induction of NaCl appetite in these strains, by using the more common Sprague-Dawley (SD) and Wistar (WS) strains for comparison. In the first experiment, LE and SD rats were administered three treatments known to induce an appetite for NaCl solution in rats. Administration of deoxycorticosterone acetate (DOCA) increased the intake of 0.45 M NaCl in both strains, but the amounts consumed were about 2-fold greater in LE rats than in SD rats. Administration of captopril also increased NaCl intake, but there were no differences between LE and SD rats. NaCl depletion with furosemide induced NaCl appetite in both strains, but the amounts consumed were about 2-fold greater in LE rats than in SD rats. In the second experiment, adult male WF and WS rats were administered DOCA, enalapril, or furosemide and NaCl appetite was determined. Both strains showed comparable NaCl appetite during each of these treatments. However, during a 5-week regimen of DOCA with only NaCl-KCl solution to drink, uninephrectomized WF rats consumed less than WS rats. Thus, despite reported resistance to MC-induced hypertension, neither LE nor WF strains of rats showed correspondingly marked deficits in induced NaCl appetite.