Pressor response to compression of the ventrolateral medulla mediated by glutamate receptors

The rostral ventrolateral medulla (RVLM) is considered a major center for t he regulation of sympathetic and cardiovascular activities. Several clinica l studies have indicated a possible causal relationship between neurovascul ar contact of the left RVLM and essential hypertension, and some investigat ors have suggested that the left RVLM is more sensitive to pulsatile compre ssion than the right RVLM. Previously, we reported that pulsatile compressi on of the RVLM elevates arterial pressure by enhancing sympathetic outflow in rats; however, we have not investigated the laterality of the responses to the compression. In addition, it remains to be elucidated whether RVLM n eurons are activated by compression and, if so, how they are activated. The refore, we performed compression experiments in rats to investigate these i ssues. Pulsatile compression was performed on the unilateral RVLM with a pu lsating probe in anesthetized and artificially ventilated rats. Pulsatile c ompression of the unilateral RVLM increased arterial pressure, heart rate, and sympathetic nerve activity. The presser response to compression was inh ibited significantly after local microinjection of glutamate receptor antag onists. Pulsatile compression of the RVLM increased Fos immunoreactivitiy, a marker of neuronal activation, within the nuclei of postsynaptic RVLM neu rons. All results were observed symmetrically. The data indicate that the r esponses to pulsatile compression of the unilateral RVLM are similar on bot h sides. They also suggest that pulsatile compression of the RVLM increases sympathetic and cardiovascular activities by activating postsynaptic RVLM neurons through the stimulation of the local glutamate receptors in rats.