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Am J Physiol Heart Circ Physiol 288: H2068-H2076, 2005. First published December 16, 2004; doi:10.1152/ajpheart.00919.2003
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Independent modification of baroreceptor and exercise pressor reflex function by nitric oxide in nucleus tractus solitarius

Scott A. Smith,1 Jere H. Mitchell,2,3 and Jianhua Li4

Departments of 1Health Care Sciences, 2Internal Medicine, and 3Physiology, Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas, Texas; and 4Division of Cardiology, Department of Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania

Submitted 26 September 2003 ; accepted in final form 13 December 2004

It has been suggested that nitric oxide (NO) is a key modulator of both baroreceptor and exercise pressor reflex afferent signals processed within the nucleus tractus solitarius (NTS). However, studies investigating the independent effects of NO within the NTS on the function of each reflex have produced inconsistent results. To address these concerns, the effects of microdialyzing 10 mM L-arginine, an NO precursor, and 20 mM NG-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor, into the NTS on baroreceptor and exercise pressor reflex function were examined in 17 anesthetized cats. Arterial baroreflex regulation of heart rate was quantified using vasoactive drugs to induce acute changes in mean arterial pressure (MAP). To activate the exercise pressor reflex, static hindlimb contractions were induced by electrical stimulation of spinal ventral roots. To isolate the exercise pressor reflex, contractions were repeated after barodenervation. The gain coefficient of the arterial cardiac baroreflex was significantly different from control (–0.24 ± 0.04 beats·min–1·mmHg–1) after the dialysis of L-arginine (–0.18 ± 0.02 beats·min–1·mmHg–1) and L-NAME (–0.29 ± 0.02 beats·min–1·mmHg–1). In barodenervated animals, the peak MAP response to activation of the exercise pressor reflex (change in MAP from baseline, 39 ± 7 mmHg) was significantly attenuated by the dialysis of L-arginine (change in MAP from baseline, 29 ± 6 mmHg). The results demonstrate that NO within the NTS can independently modulate both the arterial cardiac baroreflex and the exercise pressor reflex. Collectively, these findings provide a neuroanatomical and chemical basis for the regulation of baroreflex and exercise pressor reflex function within the central nervous system.

autonomic nervous system; arterial baroreflex



Address for reprint requests and other correspondence: J. Li, Division of Cardiology, H047, Dept. of Medicine, Pennsylvania State Univ. College of Medicine, Milton Hershey Medical Center, 500 Univ. Dr., Hershey, PA 17033 (E-mail: jzl10{at}psu.edu)




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