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Am J Physiol Heart Circ Physiol 282: H1615-H1624, 2002. First published January 17, 2002; doi:10.1152/ajpheart.00725.2001
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Vol. 282, Issue 5, H1615-H1624, May 2002

GABAA receptor activation at medullary sympathetic neurons contributes to postexercise hypotension

Radhika Kajekar1, Chao-Yin Chen1, Tatsushi Mutoh2, and Ann C. Bonham1,3

1 Department of Internal Medicine and 3 Department of Pharmacology, University of California at Davis, Davis, California 95616; and 2 Department of Anatomy and Brain Science, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan

A single bout of exercise results in a postexercise 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 gamma -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 versus 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.

spontaneously hypertensive rats; central sympathetic network; extracellular recording


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