Differential effect of central command on aortic and carotid sinus baroreceptor-heart rate reflexes at the onset of spontaneous, fictive motor activity.
Our laboratory has reported that central command blunts the sensitivity of the aortic baroreceptor-heart rate (HR) reflex at the onset of voluntary static exercise in conscious cats and spontaneous contraction in decerebrate cats. The purpose of this study was to examine whether central command attenuates the sensitivity of the carotid sinus baroreceptor-HR reflex at the onset of spontaneous, fictive motor activity in paralyzed, decerebrate cats. We confirmed that aortic nerve (AN)-stimulation-induced bradycardia was markedly blunted to 26 ± 4.4% of the control (21 ± 1.3 beats/min) at the onset of spontaneous motor activity. Although the baroreflex bradycardia by electrical stimulation of the carotid sinus nerve (CSN) was suppressed (P < 0.05) to 86 ± 5.6% of the control (38 ± 1.2 beats/min), the inhibitory effect of spontaneous motor activity was much weaker (P < 0.05) with CSN stimulation than with AN stimulation. The baroreflex bradycardia elicited by brief occlusion of the abdominal aorta was blunted to 36% of the control (36 ± 1.6 beats/min) during spontaneous motor activity, suggesting that central command is able to inhibit the cardiomotor sensitivity of arterial baroreflexes as the net effect. Mechanical stretch of the triceps surae muscle never affected the baroreflex bradycardia elicited by AN or CSN stimulation and by aortic occlusion, suggesting that muscle mechanoreflex did not modify the cardiomotor sensitivity of aortic and carotid sinus baroreflex. Since the inhibitory effect of central command on the carotid baroreflex pathway, associated with spontaneous motor activity, was much weaker compared with the aortic baroreflex pathway, it is concluded that central command does not force a generalized modulation on the whole pathways of arterial baroreflexes but provides selective inhibition for the cardiomotor component of the aortic baroreflex.
Department of Physiology, Graduate School of Health Sciences, Hiroshima University, Kasumi, Minami-ku, Hiroshima, Japan. matsuk@hiroshima-u.ac.jp
Kanji
K
Matsukawa
Kei
K
Ishii
Akito
A
Kadowaki
Nan
N
Liang
Tomoko
T
Ishida
D000818:Animals; D017704:Baroreflex; D001794:Blood Pressure; D001919:Bradycardia / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D001921:Brain / Q000503:physiopathology*; D002346:Carotid Sinus / Q000294:innervation*; D002415:Cats; D003655:Decerebrate State; D004558:Electric Stimulation; D006339:Heart Rate; D009043:Motor Activity; D009470:Muscle Spindles / Q000503:physiopathology; D009434:Neural Pathways / Q000503:physiopathology; D011311:Pressoreceptors / Q000503:physiopathology*; D012850:Sinus of Valsalva / Q000294:innervation*; D013997:Time Factors