Abstract
The rostral ventrolateral medulla (RVLM) is considered to be a major center for the regulation of sympathetic and cardiovascular activities. Several clinical studies have indicated a possible causal relationship between vasculoneural contact of the RVLM and essential hypertension. We previously reported that pulsatile compression of the ventral surface of the unilateral RVLM with a pulsating probe in anesthetized (with urethane) and artificially ventilated rats elevates arterial pressure, heart rate, and sympathetic nerve activity [28]. However, we have not investigated how and what kind of neurons are activated by compression. Therefore, we performed compression experiments in rats and examined the expression of c-fos, a marker of neuronal activation. The data indicate that after the compression of the ventral surface of the RVLM, c-fos mRNA was increased in the rostral and caudal ventrolateral medulla and the number of neurons containing specifically induced Fos-protein was considerably larger. They also suggest that the Fos-positive neurons also contain tyrosine hydroxylase, indicating that mechanical pressure (compression)-stimulated neural excitation occurred in the A1/C1 catecholamine-neurons and the specific area in the ventral surface of the RVLM is sensitive to compression.
