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Hypertension Unit, University of Ottawa Heart Institute, Ottawa, Ontario K1Y 4W7, Canada
An enhanced responsiveness
to increases in cerebrospinal fluid (CSF) Na+ by high salt
intake may contribute to salt-sensitive hypertension in Dahl
salt-sensitive (S) rats. To test this hypothesis, sympathetic and
pressor responses to acute and chronic increases in CSF Na+
were evaluated. In conscious young (5-6 wk old) and adult
(10-11 wk old) Dahl S and salt-resistant (R) rats as well as
weight-matched Wistar rats, hemodynamic [blood pressure (BP) and heart
rate (HR)] and sympathetic [renal sympathetic nerve activity (RSNA)]
responses to 10-min intracerebroventricular infusions of artificial CSF (aCSF) and Na+-rich aCSF (containing 0.2-0.45 M
Na+) were evaluated. Intracerebroventricular
Na+-rich aCSF increased BP, RSNA, and HR in a dose-related
manner. The extent of these increases was significantly larger in Dahl S versus Dahl R or Wistar rats and young versus adult Dahl S rats. In a
second set of experiments, young Dahl S and R rats received a chronic
intracerebroventricular infusion of aCSF or Na+-rich (0.8 M) aCSF (5 µl/h) for 14 days, with the use of osmotic minipumps. On
day 14 in conscious rats, CSF was sampled and BP, HR, and
RSNA were recorded at rest and in response to air stress, intracerebroventricular 
2-adrenoceptor agonist
guanabenz, intracerebroventricular ouabain, and intravenous
phenylephrine and nitroprusside to estimate baroreflex function. The
infusion of Na+-rich aCSF versus aCSF increased CSF
Na+ concentration to the same extent but caused severe
versus mild hypertension in Dahl S and Dahl R rats, respectively. After
central Na+ loading, hypothalamus "ouabain"
significantly increased in Dahl S and only tended to increase in Dahl R
rats. Moreover, sympathoexcitatory and pressor responses to
intracerebroventricular exogenous ouabain were attenuated by
Na+-rich aCSF to a greater extent in Dahl S versus Dahl R
rats. Responses to air-jet stress or intracerebroventricular guanabenz
were enhanced by Na+-rich aCSF in both strains, but the
extent of enhancement was significantly larger in Dahl S versus Dahl R. Na+-rich aCSF impaired arterial baroreflex control of RSNA
more markedly in Dahl S versus R rats. These findings indicate that
genetic control of mechanisms linking CSF Na+ with brain
"ouabain" is altered in Dahl S rats toward sympathetic hyperactivity and hypertension.
brain "ouabain"; cerebrospinal fluid sodium ion; hypertension; sympathoexcitation; guanabenz; air stress; baroreflex
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