7Recently, the authors experienced four patients who had refractory hypertension and neurovascular compression of the rostral ventrolateral medulla (RVLM). One of them, a 49-year-old woman, had undergone continuous intravenous drip injections of calcium channel blockers and b-blockers for more than 3 years because of severe and refractory hypertension. The patients had undergone microvascular decompression (MVD) of the RVLM, and the changes in blood pressure (BP) and sympathetic nerve activities were recorded. In these patients, BP decreased to the normal range without any antihypertensive drugs 2 to 3 months after MVD. The tibial sympathetic nerve activities under resting and stress conditions significantly decreased, and plasma levels of norepinephrine, urinary levels of adrenaline, and plasma renin activity were also significantly decreased after MVD of RVLM. In some patients with refractory hypertension, arterial compression of the RVLM enhances sympathetic nerve activity and renin-angiotensin system to thereby increase BP. In these patients, the operative decompression of the RVLM could lower BP via restoration of sympathetic nerve activities and the renin-angiotensin system. J Clin Hypertens (Greenwich). 2011;13:818-820. Ó2011 Wiley Periodicals, Inc.Sympathetic hyperactivity of central origin is implicated in the pathogenesis of hypertension. However, the precise mechanisms that cause central sympathetic hyperactivity remain unclear. The rostral ventrolateral medulla (RVLM) contains neurons that are the major tonic source of supraspinal sympathoexcitatory outflow to the heart, kidneys, and vessels.1 In humans, RVLM exists near the dorsal root entry zone of cranial nerves IX and X. A possible association between essential hypertension and neurovascular compression (NVC) of the RVLM has been reported by autopsy, 2 magnetic resonance imaging ⁄ magnetic resonance angiography (MRI ⁄ MRA), 3 and intraoperative observation.4 Some of these reports referred to enhanced sympathetic activities in hypertensive patients with NVC compared with hypertensive patients without NVC or normotensive patients. In rats, we reported that pulsatile compression of the RVLM leads to activation of RVLM neurons to elicit sympathetic hyperactivity and blood pressure (BP) elevation. 5 A causative relationship between NVC of the RVLM and hypertension was further ascertained by the fact that surgical microvascular decompression (MVD) substantially decreased BP in patients with refractory hypertension. 4 However, except in our case report, there has been no report that neurovascular decompression of the RVLM restores sympathetic activity to thereby decrease BP. 6 Therefore, in the present report, the effects of surgical MVD of the RVLM on BP, sympathetic nerve activities, and reninangiotensin system were explored in patients with refractory hypertension. METHODS PatientsFour patients were referred to our hospital because of refractory hypertension. Of these, 3 were women and 1 was a man, ranging in age between 35 and 51 years. Three of the...

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