Brain ‘Ouabain,’ Sodium, and Arterial Baroreflex in Spontaneously Hypertensive Rats

Abstract

Abstract To assess the possible role of brain “ouabain” in modulating arterial baroreflex function in salt-sensitive hypertension, arterial baroreflex control of renal sympathetic nerve activity and heart rate was evaluated in conscious spontaneously hypertensive rats and compared with that in Wistar-Kyoto rats. A regular sodium or high sodium diet was provided from 5 to 9 weeks of age, with intracerebroventricular infusion of antibody Fab fragments, which bind ouabainlike substances with high affinity, or, as control, nonspecific γ-globulins (200 μg · 12 μL −1 · d −1 for both). Baroreflex function was assessed by plotting changes in renal sympathetic nerve activity or heart rate against changes in mean arterial pressure by phenylephrine and nitroprusside. In control Wistar-Kyoto rats, high sodium intake did not increase resting blood pressure but sensitized baroreflex control of renal sympathetic nerve activity. In control spontaneously hypertensive rats, high sodium intake significantly increased blood pressure but did not enhance renal sympathetic nerve activity responses. However, in spontaneously hypertensive rats given high sodium diets and treated with Fab fragments, blood pressure did not increase and the baroreflex control of renal sympathetic nerve activity was sensitized significantly. We conclude that in spontaneously hypertensive rats, increase of central “ouabain” by high sodium intake prevents an increase in the sensitivity of arterial baroreflex control of renal sympathetic nerve activity, as observed in Wistar-Kyoto rats on high sodium diets.