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Frequency limits on aortic baroreceptor input to nucleus tractus solitarii

Division of Cardiovascular Medicine and Department of Pharmacology, University of California, Davis, California 95616 The frequency of baroreceptor volleys to the central nervous system can influence the fidelity of baroreceptor signal transmission and thus may affect baroreflex regulation of blood...

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Published in:American journal of physiology. Heart and circulatory physiology 2000-02, Vol.278 (2), p.H577-H585
Main Authors: Liu, Zhi, Chen, Chao-Yin, Bonham, Ann C
Format: Article
Language:English
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Summary:Division of Cardiovascular Medicine and Department of Pharmacology, University of California, Davis, California 95616 The frequency of baroreceptor volleys to the central nervous system can influence the fidelity of baroreceptor signal transmission and thus may affect baroreflex regulation of blood pressure. We examined 1 ) the extent to which frequency-dependent depression of aortic baroreceptor signals was initiated at the first central synapse between primary baroreceptor fibers and second-order nucleus tractus solitarii (NTS) neurons; 2 ) whether the pattern of baroreceptor input influenced the depression; and 3 ) the potential relevance to baroreflex sympathoinhibition. In urethan-anesthetized rats, NTS action potential responses of neurons classified as second or higher order and averaged lumbar sympathetic nerve activity responses were simultaneously measured during 100 aortic depressor nerve stimuli delivered in constant or phasic patterns (0.8-48 Hz). Frequency-dependent depression was initiated at second-order neurons, with NTS responses decreasing to a 72% response rate at 48 Hz; the depression was greater at higher-order neurons; responses decreased to a 30% response rate. The depression was slightly but significantly greater with phasic inputs. Curve fitting suggested that synaptic depression may limit baroreflex sympathoinhibition. Thus frequency limits on baroreceptor inputs at NTS synapses may affect baroreflex function. synaptic transmission; in vivo; cardiovascular; aortic depressor nerve; lumbar sympathetic nerve
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.2000.278.2.h577