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Articles in PresS, published online ahead of print January 17, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00725.2001
Submitted on August 13, 2001
Accepted on January 14, 2002
1 Internal Medicine, University of California, Davis, Davis, CA, USA
2 Anatomy and Brain Science, Kobe University, Kobe, Japan
3 Internal Medicine, University of California, Davis, Davis, CA, USA; Pharmacology, University of California, Davis, Davis, CA, USA
* To whom correspondence should be addressed. E-mail: acbonham{at}ucdavis.edu.
A single bout of exercise results in a post-exercise hypotension (PEH) that is accompanied by a reduced baroreflex function. Based on the role of rostral ventrolateral medulla (RVLM) neurons in controlling sympathetic nerve activity (SNA) and blood pressure, the role of 
-aminobutyric acid (GABA) in controlling RVLM neuronal activity, and the reduced baroreflex-SNA relationship during PEH, we determined whether: 1) RVLM neuronal activity is decreased during PEH; 2) GABAA-receptor mechanisms mediate the decrease; and 3) baroreflex control of RVLM activity is reduced. Spontaneously hypertensive rats (SHR) were subjected to 40 min of treadmill or sham-exercise (SHAM-PEH). PEH lasted 10 h in conscious and anesthetized SHR, indicating that the anesthetics did not affect the expression of PEH. Extracellular RVLM neuronal activity having a cardiac and sympathetic rhythm; lumbar SNA; and blood pressure were recorded at rest and during baroreflex function curves. Resting RVLM neuronal activity was lower and was increased to a greater extent by GABAA-receptor antagonism in PEH vs. SHAM-PEH (P < 0.05). Baroreflex control of RVLM neuronal activity operated with a reduced gain (P < 0.05). Thus, increased GABA signaling at RVLM neurons may contribute to PEH.
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