PULSATILE COMPRESSION OF THE ROSTRAL VENTROLATERAL MEDULLA IN HYPERTENSION

The rostral ventrolateral medulla (RVLM) has bee known to be a major r egulating center of sympathetic and cardiovascular activities. An asso ciation between essential hypertension and neurovascular compression o f the RVLM has been reported in clinical observations, including magne tic resonance imaging (MRI) studies. To reconfirm this relationship, w e performed MRI using a high-resolution 512 x 512 matrix in patients w ith essential and secondary hypertension and in normotensive subjects. The duration of hypertension and the degree of organ damage by hypert ension were not significantly different between the two hypertension g roups. Neurovascular compression of the RVLM was observed in 74% of th e essential hypertension group, and the incidence of compression was s ignificantly higher than in the secondary hypertension group (11%) or in the normotensive group (13%) (P < .01). These results from the clin ical studies suggest that neurovascular compression of the RVLM is, at least in part, causally related to essential hypertension. Although b lood pressure elevation by pulsatile compression of the RVLM in an exp erimental baboon model has already been reported, its underlying mecha nism is not well known. Accordingly, we performed experiments to inves tigate whether pulsatile compression of the RVLM would increase arteri al pressure and to elucidate the mechanism of the presser response in rats. Sympathetic nerve activity, arterial pressure, heart rate, and p lasma levels of epinephrine and norepinephrine were increased by pulsa tile compression of the RVLM. The presser response was abolished by in travenous treatment with hexamethonium or RVLM injection of kainic aci d. In summary, the results from the MRI studies suggest that neurovasc ular compression of the RVLM is, at least in part, causally related to essential hypertension. This was supported by the results from experi mental studies using rats indicating that pulsatile compression of the RVLM increases arterial pressure by enhancing sympathetic outflow.