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Articles in PresS, published online ahead of print October 24, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00628.2002
Submitted on July 19, 2002
Accepted on October 12, 2002
1 Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT, USA
* To whom correspondence should be addressed. E-mail: steve.bealer{at}deans.pharm.utah.edu.
Increased dietary sodium enhances both excitatory and inhibitory blood pressure responses to stimulation of the central sympathetic nervous system (SymNS) centers. In addition, long term (hrs-days) administration of angiotensin II (AngII) increases blood pressure by activation of the SymNS. These studies investigated the effects of increased dietary sodium on SymNS control of blood pressure during 0-24 hr infusion of AngII in conscious, male rats consuming either tap water (TAP) or isotonic saline (ISO) for 2-3 weeks. The SymNS component (evaluated by ganglionic blockade with trimetaphan) of both control blood pressure and the pressor response to iv AngII was reduced in ISO animals. Furthermore, although the pressor response to iv AngII infusion was similar between groups, the baroreflex-induced bradycardia during the initial 6 hr of AngII infusion was significantly greater, while the tachycardia accompanying longer infusion periods was significantly attenuated in ISO animals. These data suggest that in normal rats increased dietary sodium enhances sympathoinhibitory responses during iv AngII.
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