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(Hypertension. 2002;40:560.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Rostral Ventrolateral Medulla Neurons of Neonatal Wistar-Kyoto and Spontaneously Hypertensive Rats

Tomokazu Matsuura; Hiroo Kumagai; Akira Kawai; Hiroshi Onimaru; Masaki Imai; Naoki Oshima; Katsufumi Sakata; Takao Saruta

From the Department of Internal Medicine, Keio University School of Medicine (T.M., H.K., M.I., N.O., K.S., T.S.), Shinjuku-ku, Tokyo, Japan; and Department of Physiology, Showa University School of Medicine (A.K., H.O.), Shinagawa-ku, Tokyo, Japan.

Correspondence to Hiroo Kumagai, MD, Assistant Professor, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. E-mail hkumagai{at}sc.itc.keio.ac.jp

We compared the electrophysiological properties of neurons in the rostral ventrolateral medulla (RVLM) of neonatal Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), and responses to angiotensin II and its type 1 receptor antagonist candesartan. Using the whole-cell patch-clamp technique, we examined the characteristics of RVLM neurons in brainstem–spinal cord preparations with a preserved sympathetic neuronal network. The baseline membrane potential of irregularly firing neurons was less negative (-50.1±0.6 versus -52.0±0.6 mV) and the firing rate was faster (3.0±0.2 versus 2.0±0.2 Hz) in SHR (n=56) than in WKY (n=38). Superfusion with angiotensin II (6 µmol/L) significantly depolarized the RVLM bulbospinal neurons in SHR (5.4±1.1 mV, n=15) but not in WKY. In contrast, candesartan (0.12 µmol/L) induced a significant membrane hyperpolarization (-3.7±0.4 mV; n=14) and a decrease in the firing rate in RVLM bulbospinal neurons of SHR but not of WKY. These results suggest that endogenously generated angiotensin II binds to type 1 receptors on RVLM bulbospinal neurons, thus tonically contributing to a higher membrane potential and a faster firing rate in SHR. The electrophysiological properties of RVLM neurons and their responses to angiotensin II and candesartan differ between neonatal WKY and SHR. These differences in RVLM neurons suggest a mechanism that possibly leads to elevation in blood pressure.

Key Words: brain • rostral ventrolateral medulla • angiotensin II • receptors, angiotensin • candesartan • hyperpolarization

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