(Hypertension. 1995;25:372-376.)
© 1995 American Heart Association, Inc.
Articles |
From the Hypertension Unit, University of Ottawa (Canada) Heart Institute.
Correspondence to Frans H.H. Leenen, MD, PhD, FRCPC, Hypertension Unit, University of Ottawa Heart Institute, 1053 Carling Ave, Ottawa, Ontario K1Y 4E9, Canada.
Abstract In Dahl salt-sensitive (S) rats, high sodium intake
further desensitizes arterial baroreflex function. To assess the
possible involvement of brain "oubain," we gave Dahl S rats a
regular or high sodium diet from 4 to 7 weeks of age and administered
intracerebroventricular antibody Fab fragments, which bind ouabain with
high affinity, or
-globulins as control (200 µg/12 µL per day
for both) using osmotic minipumps. We assessed arterial baroreflex
function by plotting changes in renal sympathetic nerve activity or
heart rate against changes in mean arterial pressure of conscious rats
elicited by intravenous phenylephrine and nitroprusside. Dahl S rats on
high sodium treated with
-globulins showed a significantly higher
resting mean arterial pressure versus other rats (130 to 140 versus 95
to 105 mm Hg). In rats treated with
-globulins, high sodium
desensitized baroreflex control of renal sympathetic nerve activity
compared with rats on regular sodium (average gain: -1.88±0.12 versus
-2.73±0.13, P<.05). In contrast, in rats treated with Fab
fragments, high sodium did not increase blood pressure and did not
desensitize but slightly sensitized reflex control of renal sympathetic
nerve activity. Changes in reflex control of heart rate were similar to
those of renal sympathetic nerve activity. These data indicate that
blockade of brain "oubain" prevents sodium-induced hypertension
as well as the desensitization of the arterial baroreflex in Dahl S
rats. Increased brain "oubain" may desensitize the arterial
baroreflex and thereby facilitate the hypertension in Dahl S rats on
high sodium.
Key Words: ouabain pressoreceptors sympathetic nervous system rats, Dahl immunoglobulins, Fab sodium, dietary
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