Central infusion of L-arginine or superoxide dismutase does not alter arterial pressure in SHR

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

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Abstract

Cardiovascular responses to L-arginine and nitric oxide (NO) are augmented in the rostral ventrolateral medulla (RVLM) of spontaneously hypertensive rats (SHR), and the intravenous injection of superoxide dismutase (SOD) mimetic decreases the arterial pressure in these rats. In the present study, we examined whether the chronic central infusion of L-arginine or an SOD mimetic would reduce the blood pressure of SHR and alter responses to an NOS inhibitor or an NO donor in the RVLM. For this purpose, we administered L-arginine (SHR-Arg: 13.2 μmol/day, n = 6), a stable membrane-permeable SOD mimetic, 4-hydroxy-2,2,6,6-tetramethyl piperidine-1-oxyl (tempol) (SHR-Temp: 13.2 μmol/day, n = 6), or vehicle (SHR-C: n = 6) into the lateral ventricle of 12-week-old SHR for 2 weeks. When the rats reached 14 weeks of age, N(G)-nitro-L-arginine methyl ester (L-NAME: 10 nmol/50 nl) or NOC 18 (NO donor: 10 nmol/50 nl) was microinjected into the unilateral RVLM. Blood pressure did not decrease in any of the treatment groups (SHR-Arg: 209 ± 4 mmHg, SHR-Temp: 210 ± 6 mmHg, SHR-C: 197 ± 6 mmHg). The microinjection of L-NAME into the RVLM induced a significant increase in the mean arterial pressure (MAP) (SHR-Arg: 10-4 mmHg, SHR-Temp: 12 ± 4 mmHg, SHR-C: 11 ± 3 mmHg), and the increases in MAP did not differ among the groups. The microinjection of NOC 18 reduced MAP (SHR-Arg: -12 ± 2 mmHg, SHR-Temp: -15 ± 3 mmHg, SHR-C: -13 ± 3 mmHg), and the depressor responses were comparable among groups. These results do not support the hypothesis that chronic L-arginine deficiency or the enhanced degeneration of NO by superoxide radicals in the central nervous system contributes to the maintenance of arterial pressure in SHR.

Original languageEnglish
Pages (from-to)339-343
Number of pages5
JournalHypertension Research
Volume23
Issue number4
Publication statusPublished - Jul 2000

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Inbred SHR Rats
Superoxide Dismutase
Arginine
Arterial Pressure
NG-Nitroarginine Methyl Ester
Nitric Oxide Donors
Microinjections
Nitric Oxide
Blood Pressure
Lateral Ventricles
Intravenous Injections
Superoxides

All Science Journal Classification (ASJC) codes

  • Internal Medicine

Cite this

Kagiyama, S., Tsuchihashi, T., Abe, I., Matsumura, K., & Fujishima, M. (2000). Central infusion of L-arginine or superoxide dismutase does not alter arterial pressure in SHR. Hypertension Research, 23(4), 339-343.

Central infusion of L-arginine or superoxide dismutase does not alter arterial pressure in SHR. / Kagiyama, Shuntaro; Tsuchihashi, Takuya; Abe, Isao; Matsumura, Kiyoshi; Fujishima, Masatoshi.

In: Hypertension Research, Vol. 23, No. 4, 07.2000, p. 339-343.

Research output: Contribution to journalArticle

Kagiyama, S, Tsuchihashi, T, Abe, I, Matsumura, K & Fujishima, M 2000, 'Central infusion of L-arginine or superoxide dismutase does not alter arterial pressure in SHR', Hypertension Research, vol. 23, no. 4, pp. 339-343.
Kagiyama S, Tsuchihashi T, Abe I, Matsumura K, Fujishima M. Central infusion of L-arginine or superoxide dismutase does not alter arterial pressure in SHR. Hypertension Research. 2000 Jul;23(4):339-343.
Kagiyama, Shuntaro ; Tsuchihashi, Takuya ; Abe, Isao ; Matsumura, Kiyoshi ; Fujishima, Masatoshi. / Central infusion of L-arginine or superoxide dismutase does not alter arterial pressure in SHR. In: Hypertension Research. 2000 ; Vol. 23, No. 4. pp. 339-343.
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AB - Cardiovascular responses to L-arginine and nitric oxide (NO) are augmented in the rostral ventrolateral medulla (RVLM) of spontaneously hypertensive rats (SHR), and the intravenous injection of superoxide dismutase (SOD) mimetic decreases the arterial pressure in these rats. In the present study, we examined whether the chronic central infusion of L-arginine or an SOD mimetic would reduce the blood pressure of SHR and alter responses to an NOS inhibitor or an NO donor in the RVLM. For this purpose, we administered L-arginine (SHR-Arg: 13.2 μmol/day, n = 6), a stable membrane-permeable SOD mimetic, 4-hydroxy-2,2,6,6-tetramethyl piperidine-1-oxyl (tempol) (SHR-Temp: 13.2 μmol/day, n = 6), or vehicle (SHR-C: n = 6) into the lateral ventricle of 12-week-old SHR for 2 weeks. When the rats reached 14 weeks of age, N(G)-nitro-L-arginine methyl ester (L-NAME: 10 nmol/50 nl) or NOC 18 (NO donor: 10 nmol/50 nl) was microinjected into the unilateral RVLM. Blood pressure did not decrease in any of the treatment groups (SHR-Arg: 209 ± 4 mmHg, SHR-Temp: 210 ± 6 mmHg, SHR-C: 197 ± 6 mmHg). The microinjection of L-NAME into the RVLM induced a significant increase in the mean arterial pressure (MAP) (SHR-Arg: 10-4 mmHg, SHR-Temp: 12 ± 4 mmHg, SHR-C: 11 ± 3 mmHg), and the increases in MAP did not differ among the groups. The microinjection of NOC 18 reduced MAP (SHR-Arg: -12 ± 2 mmHg, SHR-Temp: -15 ± 3 mmHg, SHR-C: -13 ± 3 mmHg), and the depressor responses were comparable among groups. These results do not support the hypothesis that chronic L-arginine deficiency or the enhanced degeneration of NO by superoxide radicals in the central nervous system contributes to the maintenance of arterial pressure in SHR.

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