Abstract 416: Chloride Ion Contributes to the Hypertension Induced by Central NaCl
Previous studies in salt-sensitive animal strains suggest that an increase in the level of sodium in the cerebrospinal fluid (CSF [Na]) is crucial for the development of hypertension induced by a high salt diet. Although chronic intracerebroventricular (icv) infusions of NaCl-rich artificial CSF (NaCl-rich aCSF) are frequently used to study the mechanisms of the hypertension caused by high salt diet and/or elevated CSF [Na], the contribution of chronic increased CSF [Cl] to the hypertensive response has not been examined. In the present study, we compared the effects on blood pressure of chronic (10 day) icv infusions of NaCl-rich aCSF vs. similar infusions in which excess Na+ or Cl- was substituted with another ion in wild-type (WT) mice and in knockout/knockin mice with a ouabain-resistant endogenous Na, K-ATPase α2 subunit (α2R/R). The latter mice are known to lack a pressor response to icv NaCl-rich aCSF. Mean arterial pressure (MAP) and heart rate (HR) on day 10 of infusion were (mean ± S.E.M., n = 4-5 per group:
These studies suggest that both elevated CSF [Na] and CSF [Cl] contribute to the pressor response to increased CSF [NaCl] via a common mechanism: binding of endogenous ouabain to the Na, K-ATPase α2 isoform.
- © 2012 by American Heart Association, Inc.