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(Hypertension. 1996;28:224-227.)
© 1996 American Heart Association, Inc.

Articles

Angiotensin II Increases Norepinephrine Turnover in the Anteroventral Third Ventricle of Spontaneously Hypertensive Rats

Akira Tsukashima; Takuya Tsuchihashi; Isao Abe; Kaoru Nakamura; Hideyuki Uchimura; Masatoshi Fujishima

the Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka City (A.T., T.T., I.A., M.F.), and Hizen National Mental Hospital, Center for Emotional and Behavioral Disorder (K.N., H.U.), Kanzaki, Saga, Japan.

Correspondence to Akira Tsukashima, MD, Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka City 812, Japan.

We evaluated the effect of angiotensin II (Ang II) administered by intracerebroventricular injection on norepinephrine turnover in the anteroventral third ventricle in adult spontaneously hypertensive rats (SHR, n=35) and age-matched Wistar-Kyoto rats (WKY, n=38). Ang II (100 ng) or saline (vehicle control) was administered into the cerebral ventricle 30 minutes after injection of -methyl-p-tyrosine (250 mg/kg IP). Norepinephrine turnover was assessed by evaluation of the norepinephrine concentration before and 1 hour after such administration. The pressor response to Ang II administration was significantly greater in SHR than in WKY (+43±3 versus +23±2 mm Hg, P<.01). Baseline norepinephrine turnover (response to saline) was reduced in the ventral median preoptic nucleus of SHR. Ang II significantly increased norepinephrine turnover in the organum vasculosum lamina terminalis and ventral median preoptic nucleus of SHR (organum vasculosum lamina terminalis: 40±5% by Ang II versus 18±6% by saline, P<.05; ventral median preoptic nucleus: 32±3% by Ang II versus 21±2% by saline, P<.05) but not of WKY (37±5% versus 29±5%, P=NS, and 30±2% versus 32±3%, P=NS, respectively). Thus, norepinephrine turnover in the anteroventral third ventricle region induced by intracerebroventricular administration of Ang II was increased in SHR. This effect may contribute to the enhanced pressor response to central Ang II seen in this model.

Key Words: angiotensin II • brain • hypertension, genetic • norepinephrine • nervous system • rats, inbred SHR

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