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This Article Full Text Full Text (PDF) All Versions of this Article: 294/6/R1863    most recent 00757.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Kleiber, A. C. Articles by Patel, K. P. Search for Related Content PubMed PubMed Citation Articles by Kleiber, A. C. Articles by Patel, K. P.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Exercise training normalizes enhanced glutamate-mediated sympathetic activation from the PVN in heart failure

¹Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; and ²Department of Pharmacology, Midwestern University, Downers Grove, Illinois

Submitted 17 October 2007 ; accepted in final form 26 March 2008

Exercise training (ExT) normalizes the increased sympathetic outflow in heart failure (HF), but the mechanisms are not known. We hypothesized that ExT would normalize the augmented glutamatergic mechanisms mediated by N-methyl-D-aspartic acid (NMDA) receptors within the paraventricular nucleus (PVN) that occur with HF. Four groups of rats were used: 1) sham-operated (Sham) sedentary (Sed), 2) Sham ExT, 3) HF Sed, and 4) HF ExT. HF was induced by left coronary artery ligation, and ExT consisted of 3 wk of treadmill running. In -chloralose-urethane-anesthetized rats, the increase in renal sympathetic nerve activity in response to the highest dose of NMDA (200 pmol) injected into the PVN in the HF Sed group was approximately twice that of the Sham Sed group. In the HF ExT group the response was not different from the Sham Sed and Sham ExT groups. Relative NMDA NR1 receptor subunit mRNA expression was 63% higher in the HF Sed group compared with the Sham Sed group but in the HF ExT group was not different from the Sham Sed and Sham ExT groups. NR1 receptor subunit protein expression was increased 87% in the HF Sed group compared with the Sham Sed group but in the HF ExT group was not significantly different from the Sham Sed and Sham ExT groups. Thus one mechanism by which ExT alleviates elevated sympathetic outflow in HF may be through normalization of glutamatergic mechanisms within the PVN.

paraventricular nucleus; N-methyl-D-aspartic acid receptors; sympathetic nerve activity

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