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(Hypertension. 1998;31:1030-1034.)
© 1998 American Heart Association, Inc.

Scientific Contributions

Enhanced Depressor Response to Nitric Oxide in the Rostral Ventrolateral Medulla of Spontaneously Hypertensive Rats

Shuntaro Kagiyama; Takuya Tsuchihashi; Isao Abe; ; Masatoshi Fujishima

From the Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

Correspondence to Shuntaro Kagiyama, MD, Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Maidashi 3–1-1, Higashi-ku, Fukuoka 812–8582, Japan. E-mail kagiyama{at}intmed2.med.kyushu-u.ac.jp

Abstract—Possible impairment of the L-arginine–nitric oxide (NO) pathway in the rostral ventrolateral medulla of adult spontaneously hypertensive rats (SHR) was investigated by microinjecting N^G-nitro-L-arginine methyl ester (L-NAME), NOC 18 (an NO donor), or L-arginine. Unilateral injection of L-NAME (10 nmol/50 nL) into the rostral ventrolateral medulla significantly increased mean arterial pressure (MAP) in both SHR and Wistar-Kyoto rats (WKY). The increases in MAP did not differ significantly between the two strains (15±3 versus 10±2 mm Hg, respectively; n=8). In contrast, microinjection of L-arginine elicited significant (P<.05) dose-dependent decreases in MAP in both strains, and these depressor responses were significantly greater in SHR than in WKY (in 10 nmol of L-arginine: –29±2 versus –15±2 mm Hg, respectively; n=8, P<.01). Similarly, microinjection of NOC 18 (10 nmol/50 nL) reduced MAP in both strains, and the depressor response was also significantly greater in SHR than in WKY (–38±7 versus –22±3 mm Hg, respectively; n=8, P<.05). These results suggest that the L-arginine–NO pathway in the rostral ventrolateral medulla is impaired in SHR and that this impairment may contribute to the increase in arterial pressure in this animal model of genetic hypertension.

Key Words: L-arginine • NOC 18 • L-NAME • medulla oblongata • microinjection

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