ARTERIAL COMPRESSION OF THE VENTROLATERAL MEDULLA

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Arterial compression of area(s) along the retro-olivary sulcus of the ventro-lateral medulla has a role in sympathetically mediated (neurogenic) hypertension. Specific Aims: 1. The primary objective of the first study is to generate a 'normal' map of the locations along the ventro-lateral medullary surface (VLMS) that produce pressor responses to stimulation (First 3 years): More specifically, the pressor-sensitive regions of the VLMS will be mapped using direct electrical stimulation during posterior fossa surgery. The location of such areas will be recorded, i.e., mapped, onto magnetic resonance images (MRI). Evidence suggests that these areas may be similarly responsive to both electrical stimulation and arterial compression. The direct effects of electrical stimulation of the VLMS on sympathetic tone and cardiovascular parameters (systemic blood pressure (BP), heart rate (HR), and arterial wall compliance) will be quantified. Sympathetic tone will be quantified by measuring muscle sympathetic nerve activity (MSNA) and plasma norepinephrine. 2. We plan to show an association between MRI evident arterial compression of pressor-sensitive areas of the VLMS (based on the 'normal' map in the first study) and sympathetic dependency of elevated BP (neurogenic hypertension). (Last 2 years): In a separate group of subjects with essential hypertension, A secondary aim in this study will be to determine if the patterns of neurogenic activation are similar in hypertensive patients with arterial compression of the VLMS and in normotensive subjects with electrical stimulation of the same anatomic locations. The findings in patients with neurovascular compression will be compared with the patterns of neurogenic and hemodynamic responses obtained during electrical stimulation of similar sites in the VLMS (from the first study). These studies will be useful in linking mechanisms underlying the pressor response to acute electrical stimulation of the VLMS with those producing sustained hypertension in patients with vascular compression of the same anatomic sites of the brainstem.