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

Abstract

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.

Resetting blood pressure by a closed-loop implanted chip system in normotensive rats

“…We observed that hypotension induced by the chip system was accompanied by significant bradycardia, which was caused by increased afferent activity of the ADN, and subsequent inhibition of sympathetic nerves and excitation of vagi (Cravo and Morrison, 1993;Aicher et al, 2000;Nosaka et al, 2000). The present study showed that the treatment with either methyl atropine or vagotomy blocked the bradycardia completely but produced no significant effect on hypotension induced by the chip system compared with the control group, and that MAP could still be satisfactorily maintained in the artificial set point level.…”

α-2 Adrenergic Transmission and Human Baroreflex Regulation

“…Stimulation of presynaptic ␣-2 adrenoceptors may modulate acetylcholine release from cholinergic neurons innervating the heart. 32 Remarkably, clonidine changed the relationship between systolic BP changes and cardiac stroke volume. With placebo, stroke volume increased as RR interval increased.…”

“…31 Decreased activity in this area may lead to a secondary increase in parasympathetic activity. 32 It is also possible that clonidine directly influences other areas in the brain stem like vagal nuclei or the caudal ventrolateral medulla. Indeed, ␣-2 adrenoreceptors are highly expressed in vagus motor nuclei in animals and in humans.…”

Effect of Atropine or Atenolol on Cardiovascular Responses to Novelty Stress in Freely-Moving Rats

“…The early bradycardia could be a baroreflex-mediated attempt to counteract the rapidly rising blood pressure. Within 2 min, this vagal activation is reversed into vagal inhibition, either by rapid resetting of baroreceptors (Dorward and Korner, 1987;Hatton et al, 1997) or centrally mediated mechanisms overriding the baroreflex (Djojosugito et al, 1970;Nosaka et al, 2000). In methylatropine-treated rats, these changes in vagal activity are blocked, leading to a very rapid increase in heart rate (no vagal activation to counteract the tachycardia) to a plateau significantly below that found in saline-treated controls (no vagal inhibition).…”