Abstract--Dahl salt-sensitive rats show increased Na⁺ entry into the brain on high salt intake and increased sympathetic and pressor responses to central Na⁺. We examined C10QTL2 and C17QTL to test whether they contribute to these phenotypes. In Dahl salt-sensitive, Lewis, and C10S.L16, and C17S.L2 congenic rats on a high salt diet for 8 to 10 days, blood pressure and heart rate were higher in Dahl salt-sensitive versus others and in C10S.L16 and C17S.L2 versus Lewis rats. Cerebrospinal fluid [Na⁺] increased by 5 mmol/L in Dahl salt-sensitive, C10S.L16, and C17S.L2 compared with Lewis rats. In rats on a regular salt diet, 8-minute intracerebroventricular infusions of artificial cerebrospinal fluid with increasing [Na⁺] caused increases in blood pressure, heart rate, and renal sympathetic nerve activity, which were 90% larger in Dahl salt-sensitive and C17S.L2 versus Lewis rats and only 35% to 45% larger in C10S.L16 versus Lewis rats. In another set of rats on regular salt, blood pressure and heart rate were recorded by telemetry before and during intracerebroventricular infusion of Na⁺-rich cerebrospinal fluid for 14 days. Na⁺-rich cerebrospinal fluid caused significantly larger increases in blood pressure and heart rate, larger responses to air stress and more impairment of baroreflex in Dahl salt-sensitive and C17S.L2 rats versus Lewis rats. In contrast, responses in C10S.L16 rats were similar to those in Lewis rats. These data suggest that, in Dahl salt-sensitive rats, genetic variants in C10QTL2 but not C17QTL contribute to increased neuronal responsiveness to cerebrospinal fluid [Na⁺]. However, neither of them contributes to the increase in cerebrospinal fluid [Na⁺] induced by high salt.