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(Hypertension. 2007;49:1315.)
© 2007 American Heart Association, Inc.
Original Articles |
From the University of Ottawa Heart Institute (B.S.H., M.A., F.H.H.L.), Ottawa, Ontario, Canada; and the Research Centre-Centre Hospitalier de lUniversité de Montréal (A.Y.D.), Université de Montréal, Montréal, Quebec, Canada.
Correspondence to Frans H.H. Leenen, Hypertension Unit, University of Ottawa Heart Institute, H360, 40 Ruskin St, Ottawa, Ontario K1Y 4W7, Canada. E-mail fleenen{at}ottawaheart.ca
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.
Key Words: brain sodium sympathetic activity blood pressure telemetry congenic strains of Dahl rats
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