Neurovascular compression: sympathetic activity in severe arterial hypertension

Abstract

Compression of the rostral ventrolateral medulla oblongata (RVLM) by an abnormally located artery is regarded as one possible cause of arterial hypertension. There exists a limited set of data suggesting that increased sympathetic activity in patients with RVLM compression may lead to arterial hypertension. Accordingly, we decided to assess the sympathetic activity in patients with severe arterial hypertension and to investigate any correlation with the presence of RVLM compression. Sixty-four patients with severe arterial hypertension were enrolled in our study. Sympathetic activity was evaluated using 24-hour urinary norepinephrine as measured by high-pressure liquid chromatography with electrochemical detection. The presence of RVLM compression was assessed with magnetic resonance imaging. Neurovascular compression of the RVLM was identified in 40 patients, 27 of whom presented left-sided compression. Twenty-four hour urinary norepinephrine averaged 263.6+/-135.9 nmol in patients with neurovascular compression - 255.6+/-137.3 nmol in those with left-sided compression and 251.6+/-138.5 nmol in patients without RVLM compression. We did not identify any increase in urinary norepinephrine in patients with severe arterial hypertension and neurovascular compression of the RVLM. Our results do not support the hypothesis that neurovascular compression of RVLM may exhibit a sympathetically mediated increase in blood pressure.