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1 Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska, United States
2 Dept. of Cellular & Integ. Physiology, University of Nebraska Medical Ctr, Theodore F. Hubbard Professor of Cardiovascular Research, Omaha, Nebraska, United States
* To whom correspondence should be addressed. E-mail: izucker{at}unmc.edu.
Exercise training (EX) has become an important modality capable of enhancing the quality of life and survival of patients with chronic heart failure (CHF). While we have shown that 4 weeks of EX in CHF evokes a reduction in renal sympathetic nerve activity (RSNA), angiotensin II (Ang II) plasma levels, and an enhancement in baroreflex sensitivity (BRS) at rest it is unclear if these phenomena are causally related. CHF was induced in rabbits by ventricular pacing (360-380 bpm) for 3 weeks. CHF rabbits were EX for 4 wks at 15-18 m/min, 6 days/wk, 30-40 min/day. Three groups of rabbits were studied; CHF, CHF-EX, and CHF-EX where Ang II levels were kept at or near levels observed in CHF non-EX rabbits by subcutaneous osmotic minipump infusion. EX prevented the increase in plasma Ang II in CHF rabbits. CHF non-EX and CHF-EX rabbits with Ang II infusion had a significantly depressed BRS slope (p<0.01 for SNP and p<0.001 for PE) and a higher baseline RSNA when compared to CHF-EX animals. EX down-regulated mRNA and protein expression of Ang II type 1 receptors in the rostral ventrolateral medulla in CHF rabbits. This was prevented by Ang II infusion. These data are consistent with the view that the reduction in sympathetic nerve activity and the improvement in baroreflex function in CHF following EX is due to the concomitant reduction in Ang II and angiotensin receptors in the central nervous system.
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