MORIMOTO Satoshi
Department School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine Position Associate Professor |
|
Article types | Original article |
Language | English |
Peer review | Peer reviewed |
Title | Neurovascular decompression of the rostral ventrolateral medulla decreases blood pressure and sympathetic nerve activity in patients with refractory hypertension. |
Journal | Formal name:Journal of clinical hypertension (Greenwich, Conn.) Abbreviation:J Clin Hypertens (Greenwich) ISSN code:17517176/15246175 |
Domestic / Foregin | Foregin |
Volume, Issue, Page | 13(11),pp.818-20 |
Author and coauthor | Sasaki Susumu, Tanda Shuji, Hatta Tsuguru, Morimoto Satoshi, Takeda Kazuo, Kizu Osamu, Tamaki Shinji, Saito Mitsuru, Tamura Yoji, Kondo Akinori |
Publication date | 2011/11 |
Summary | Recently, 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 β-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. |
DOI | 10.1111/j.1751-7176.2011.00522.x |
PMID | 22051426 |