Inhibition Of Rostral Ventrolateral Medulla Research Articles

Altered regulation of sympathetic nerve activity by the caudal ventrolateral medulla in rats after exposure to chronic intermittent hypoxia

After exposure to CIH, rats have elevated sympathetic nerve activity (SNA) and arterial pressure (AP). In addition, we have observed that rats exposed to CIH have reduced GABAergic inhibition of rostral ventrolateral medulla (RVLM), the source of drive for SNA. The caudal ventrolateral medulla (CVLM) is the major source of tonic inhibitory input to the RVLM. Here, we determined whether exposure to CIH reduces tonic CVLM‐mediated inhibition of SNA. Rats (8 wks old) were exposed to CIH (6% O2 for 40s, every 9 min, 8h/day, 2 wks). Then rats were ventilated, paralyzed, and prepared to record AP and splanchnic SNA. Under chloralose anesthesia rats subjected to CIH (n=9) vs. controls (n=7) had higher SNA (1.9 ± 0.2 vs. 0.9 ± 0.2 μV, P<0.05). Stimulation of CVLM by microinjection of glutamate (1 nmol/50 nl) virtually eliminated SNA (93 ± 3 vs. 94 ± 3 %) and produced bigger decreases in mean AP in CIH‐exposed rats (−39 ± 4 vs. −21 ± 3 mmHg, P<0.05). In contrast, inhibition of glutamatergic inputs to CVLM (kynurenate; 5.4 nmol/50 nl) evoked smaller rises in SNA in CIH rats (n=9) vs. control rats (n=7; 361 ± 63 vs. 605 ± 84 %, P < 0.05). These results suggest that the higher SNA in rats subjected to CIH can be eliminated by activation of the CVLM, likely via inhibition of an elevated drive from the RVLM. Furthermore, a reduced tonic inhibitory influence from the CVLM may contribute to the elevated SNA observed in rats after CIH. Support: NIHHL075174.

Nucleus Raphe Pallidus in EA inhibition of rostral ventrolateral medulla and cardiovascular excitatory responses

EA at P5‐6 acupoints (median nerve) excites the arcuate nucleus and ventrolateral periaqueductal gray (vlPAG), and inhibits sympathetic cardiovascular rostral ventrolateral medulla (rVLM) neurons and associated reflex responses. The present study investigated the role of the NRP in EA inhibition of rVLM neurons and whether EA and activity from the vlPAG to the rVLM passes through the NRP. In [alpha]‐chloralose anesthetized cats the splanchnic nerve (SN) was stimulated to induce cardiovascular sympathoexcitatory reflexes and EA was applied at P 5‐6 acupoints. A recording electrode was inserted into the NRP or rVLM. Microinjection of dl‐homocysteic acid (DLH), but not normal saline (NS), into vlPAG increased the NRP neuronal response to SN stimulation (5±1 to 12±1 spikes/30 stim). EA at P 5‐6 for 30 min increased the NRP response to SN stimulation (5±1 to 14±3 spikes/30 stim). EA excitation of the NRP response was blocked by microinjection of kynurenic acid (KYN) into the caudal vlPAG. Furthermore, the reflex increase in BP induced by application of bradykinin on gallbladder and the rVLM neuronal response to SN stimulation was inhibited (~58%) by injection of DLH into the vlPAG, a response that could be blocked by injection of KYN into the NRP. Thus, EA activates the arcuate and vlPAG, which excites the NRP and, in turn, inhibits the rVLM activity and sympathoexcitatory cardiovascular reflex responses. (HL‐63313)

Baroreflex independent GABAergic inhibition of rostral ventrolateral medulla (RVLM) is greater in pregnant than virgin rats: Role of angiotensin AT 1 receptors

Baroreflex independent GABAergic inhibition of rostral ventrolateral medulla (RVLM) is greater in pregnant than virgin rats: Role of angiotensin AT ₁ receptors

Regulation of sympathetic tone and arterial pressure by the rostral ventrolateral medulla after depletion of C1 cells in rats.

This review describes experiments designed to determine the role of bulbospinal (BS) C1 cells in regulating the sympathetic outflow and blood pressure. This goal was achieved by analyzing the physiological consequences of destroying BS C1 cells. These cells were destroyed by suicide transport of an anti-dopamine-beta-hydroxylase antibody conjugated to saporin (anti-D beta H-SAP). Two to 3 weeks after spinal cord injection (T2-T6), the toxin destroyed 75-85% of BS C1 and C3 cells along with > 95% of BS noradrenergic neurons (A5, A6, A7). The toxin spared BS noncatecholaminergic cells. Under anesthesia, toxin-treated rats had a normal blood pressure and an apparently normal sympathetic nerve discharge (SNA, splanchnic), and intravenous clonidine caused a normal degree of sympathoinhibition. Inhibition of rostral ventrolateral medulla (RVLM) neurons by bilateral injection of muscimol caused the same hypotension and sympathoinhibition as in control rats. The baroreflex range was 41% attenuated by the toxin, but the MAP50 was unchanged. Sympathoexcitatory responses to stimulation of peripheral chemoreceptors with cyanide or to electrical stimulation of RVLM were severely depressed (60% to 80%) in toxin-treated rats. Rats in which A5 neurons were selectively destroyed had no deficit in the parameters tested. Unit recordings of BS RVLM neurons indicated that the toxin destroyed most barosensitive C1 neurons, but spared noncatecholaminergic lightly myelinated BS cells. In summary, the integrity of C1 neurons is not essential for the generation of SNA and the maintenance of BP under resting conditions, perhaps because these functions are performed primarily by noncatecholaminergic BS neurons. However, the deficits caused by treatment with anti-D beta H-SAP indicate that BS C1 neurons play a crucial role in several sympathoexcitatory responses mediated by the RVLM.