Cardiovascular responses to glutamate and angiotensin II in ventrolateral medulla of hypertension induced by chronic inhibition of nitric oxide

Takuya Tsuchihashi, Shuntaro Kagiyama, Kiyoshi Matsumura, Yingzi Lin, Isao Abe, Masatoshi Fujishima

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

It has been suggested that nitric oxide (NO) influences the actions of L-glutamate and angiotensin II in the brain. In the present study, we examined whether cardiovascular responses to L-glutamate and angiotensin II would be altered in the rostral ventrolateral medulla (RVLM) of rats treated with an NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME). Wistar rats were treated with either L-NAME (100 mg/kg/day, n = 9) or vehicle (n = 8) for 4 weeks. L-glutamate (2 nmol/50 nl) or angiotensin II (100 pmol) was then microinjected into unilateral RVLM of anesthetized rats. Upon completion of the experiments, angiotensin-converting enzyme (ACE) activity of the brain stem was measured. The systolic blood pressure after 4 weeks of the treatment was significantly higher in the L-NAME group (203 ± 8 mmHg) than in the control group (142 ± 3 mmHg, p < 0.01). The pressor response to L-glutamate microinjected into the RVLM was significantly greater in the L-NAME group (31 ± 2 mmHg) than in the control group (24 ± 1 mmHg, p < 0.01). Similarly, angiotensin II showed a greater pressor response in the L-NAME group. ACE activity of the brain stem did not differ between the groups. In conclusion, NO may have an inhibitory influence on the actions of L-glutamate and angiotensin II in the RVLM.

Original languageEnglish
Pages (from-to)359-364
Number of pages6
JournalHypertension Research
Volume23
Issue number4
DOIs
Publication statusPublished - Jul 2000

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

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