(Hypertension. 1999;33:32-35.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
30 minutes. Peak decreases in BP, renal sympathetic nerve activity,
and HR in response to both doses of nifedipine were
significantly larger in SHR on high versus regular salt.
Nifedipine administered intravenously also
decreased BP but, in contrast, caused (reflex) increases in renal
sympathetic nerve activity and HR. On both diets,
intracerebroventricular vehicle did not
affect mean arterial pressure, renal sympathetic nerve
activity, or HR. These data indicate that in contrast to its
peripheral vasodilator effect, centrally administered
nifedipine may decrease sympathetic outflow and therefore
BP and HR. The enhanced sympathoinhibitory and depressor
responses to nifedipine in SHR on high versus regular salt
suggest that the sympathetic hyperactivity induced by high salt intake
is dependent on neuronal calcium influx via L-type channels.
Key Words: nifedipine dihydropyridines nervous system, sympathetic hypertension rats, inbred SHR sodium, dietary
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