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Central Command suppresses the cardiac bradycardia evoked by the aortic baroreflex
Author(s) -
Degtyarenko Alexandr M.,
Kaufman Marc P.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1408-b
The baroreceptor reflex, which functions to maintain arterial pressure at a constant level, is reset upwards during exercise. Central command is one of the neural mechanisms believed to cause this resetting. The evidence for this belief arises for most part from studies in which muscle contraction is possible. This prompted us to perform experiments on paralyzed decerebrated cats in which central command was evoked by stimulation of the mesencephalic locomotor region (MLR). We found that the cardiac component of the baroreceptor reflex, which was evoked by intravenous phenylephrine injection, was suppressed by MLR stimulation. Specifically, the heart rate slowing evoked by phenylephrine i.v. injection decreased by 31.8 ± 4.4 % during MLR stimulation (P <0.001, n=16). Phenylephrine injection before MLR stimulation increased mean arterial pressure by 79 ± 7% and decreased heart rate by 36 ± 5% (P< 0.001). Stimulation of the MLR following phenylephrine injection caused heart rate to return towards its baseline level even though arterial pressure remained elevated. We also found that the excitatory responses of cells in the nucleus tractus solitarius (NTS) to phenylephrine injection were suppressed by MLR stimulation. On average, the mean frequency of cells discharges was decreased by 3.8 ± 1.1 and 10.4 ± 1.8 impulses /s (P<0.005, n=14) during MLR stimulation before and after phenylephrine i.v. injection, respectively. We conclude that the NTS may be one of the sites whereby input from baroreceptors is suppressed, thereby causing the resetting to occur.