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1 Department of Pharmacology and Toxicology, College of Pharmacy, University of Utah, Salt Lake City, UT, USA
* To whom correspondence should be addressed. E-mail: steve.bealer{at}deans.pharm.utah.edu.
The present studies investigated the effects of increased dietary sodium on the modification of cardiac baroreflex responses induced by acute sodium loading. Changes in blood pressure and heart rate during iv phenylephrine and nitroprusside were compared using a 4-parameter sigmoid logistic function before and following a 30 min infusion of 0.6 M or 1.0 M NaCl in conscious Male Sprague-Dawley rats consuming only tap water (TAP) or isotonic saline (ISO) for 2-3 weeks. In TAP animals, infusion of 1.0 M NaCl increased the baroreflex-induced heart rate minimum, reduced heart rate range, and increased the operating blood pressure. In contrast, infusion of 0.6 M NaCl in TAP rats reduced both heart rate minimum and maximum. However, infusion of 0.6 M NaCl in ISO animals produced responses similar to TAP rats infused with 1.0 M NaCl. In addition, the decreased heart rate minimum in TAP rats following infusion of 0.6 M NaCl was prevented by iv administration of a vasopressin V1 receptor antagonist. Furthermore, cardiac parasympathetic responses were similar in TAP and ISO rats before and following 0.6 M NaCl infusion. However, in animals receiving iv atropine, 0.6 M NaCl decreased heart rate minimum and maximum in TAP animals, but did not alter the response parameters in ISO rats. These results demonstrate the facilitation of cardiac baroreflex responses normally observed during moderate sodium loading is mediated by vasopressin, and that increased dietary sodium ingestion reverses this facilitation by reducing sympathetic nervous system withdrawal.
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