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Am J Physiol Heart Circ Physiol 279: H1239-H1247, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 3, H1239-H1247, September 2000

Inhibition of baroreflex vagal bradycardia by activation of the rostral ventrolateral medulla in rats

Shoichiro Nosaka1, Keiko Murata1, Masayoshi Kobayashi1,2, Zhi Bin Cheng1, and Junko Maruyama1

Departments of 1 Physiology and 2 Otorhinolaryngology, Mie University School of Medicine, Tsu, Mie 514-8507, Japan

In stressful conditions, baroreflex vagal bradycardia (BVB) is often suppressed while blood pressure is increased. To address the role of the rostral ventrolateral medulla (RVL), a principal source of sympathetic tone, in inhibition of BVB, we microinjected DL-homocysteic acid (DLH, 6 nmol) into the RVL of chloralose-urethan-anesthetized, sinoaortic-denervated rats to examine the effect on BVB. The BVB was provoked by electrical stimulation of the aortic depressor nerve ipsilateral to the injection sites. DLH microinjection was found to suppress BVB while increasing blood pressure. The inhibition of BVB was observed even during the early phase in which DLH transiently suppressed central inspiratory activity. The inhibition was not affected either by upper spinal cord transection or suprapontine decerebration. Similar results were obtained by microinjection of bicuculline methiodide (160 pmol), a GABA antagonist, into the RVL of carotid sinus nerve-preserved rats due to withdrawal of a tonic GABA-mediated, inhibitory influence including the input from arterial baroreceptors. In conclusion, activation of the RVL inhibits BVB at brain stem level independently of central inspiratory drive.

aortic depressor nerve; DL-homocysteic acid; gamma -aminobutyric acid; bicuculline; sympathetic-parasympathetic interaction


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