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AJP - Heart and Circulatory Physiology, Vol 270, Issue 3 1054-H1062, Copyright © 1996 by American Physiological Society
ARTICLES |
T. Kubo, T. Imaizumi, Y. Harasawa, S. Ando, T. Tagawa, T. Endo, M. Shiramoto and A. Takeshita
Research Institute of Angiocardiology and Cardiovascular Clinic, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
While electrically stimulating the aortic depressor nerve (ADN) pseudorandomly, we recorded renal sympathetic nerve activity (RSNA) and systemic arterial pressure (SAP) in 19 alpha-chloralose-anesthetized rabbits with sinoaortic denervation. From the recorded signals, we determined the transfer functions from ADN stimulation by a pseudorandom binary sequence to RSNA [HCMD.RSNA(f)] and to SAP [HCMD.SAP(f)]. The modulus of HCMD.RSNA(f) was flat over 0.0122-0.8 Hz, whereas the phase lag increased linearly with frequency. Thus the central transduction appeared not to modify the relative amplitude of the signals from the baroreflex afferents but to provide a fixed time delay (approximately 400 ms). In contrast, the modulus of HCMD.SAP(f) decreased precipitously toward high frequencies, and the degree of the phase lag was larger than that of HCMD.RSNA(f). We conclude that 1) the transfer property of the central are does not significantly modify the relative amplitude of the frequency components of the baroreflex afferents but provides a fixed time delay and 2) the frequency independence of the modulus of the transfer property is not preserved when the analysis is extended to SAP.
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