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(Hypertension. 1995;25:814-817.)
© 1995 American Heart Association, Inc.
Articles |
From the Hypertension Unit, University of Ottawa (Ontario, Canada) Heart Institute.
Correspondence to Frans H.H. Leenen, MD, PhD, FRCPC, Hypertension Unit, University of Ottawa Heart Institute, 1053 Carling Ave, Ottawa, Ontario, Canada K1Y 4E9.
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
-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.
Key Words: ouabain pressoreceptors sympathetic nerve activity rats, SHR sodium
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