一氧化氮合酶抑制剂对有意识大鼠血管紧张素II加压反应的影响。

Artery Pub Date : 1998-01-01
T Maeda, T Yoshimura, A Ohshige, H Koyama, M Ito, H Okamura
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引用次数: 0

摘要

目的:探讨ng -单甲基- l-精氨酸(L-NMMA)和l-精氨酸(L-Arg)对大鼠血管紧张素ⅱ输注后升压反应的影响。方法:采用微型渗透泵等速腹腔注射L-NMMA和L-Arg。L-NMMA组每日输注L-NMMA (3 mg/d),连续13 d; L-NMMA + L-Arg组每日输注L-NMMA (3 mg/d),连续4 d; L-NMMA + L-Arg (12 mg/d),连续9 d。假手术大鼠作为对照。第13天麻醉,置导管于股动脉和股静脉内。在动物麻醉恢复后,在麻醉恢复后测定静脉注射血管紧张素II(50、100、200和400 ng/kg)的升压反应。结果:虽然基线平均动脉血压不受L-NMMA的影响,但与对照组相比,在剂量为50、100和200 ng/kg时,L-NMMA组对血管紧张素II的升压反应显著增加。L-NMMA加L-Arg组的疗效与对照组无显著差异。结论:一氧化氮合酶抑制剂在不足以产生高血压的剂量下,可增加血管紧张素II的升压反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of a nitric oxide synthase inhibitor on pressor response to angiotensin II in conscious rats.

Objective: We sought to characterize the effects of NG-monomethyl-L-arginine (L-NMMA) and L-arginine (L-Arg) on the pressor response to the infusion of angiotensin II in rats.

Methods: L-NMMA and L-Arg were infused intraperitoneally into rats at a constant rate by means of an osmotic minipump. The L-NMMA group received an infusion of L-NMMA (3 mg/d) daily for 13 d, whereas the L-NMMA plus L-Arg group received L-NMMA (3 mg/d) daily for 4 d, followed by L-NMMA plus L-Arg (12 mg/d) daily for 9 d. Sham operated rats served as controls. The animals were anesthetized on day 13, and catheters were placed into the femoral artery and vein. After the animals had recovered from the anesthesia, the pressor response to intravenous bolus doses of angiotensin II (50, 100, 200, and 400 ng/kg) were determined after recovery from anesthesia.

Results: While the baseline mean arterial blood pressure was not affected by L-NMMA, with or without L-Arg, the pressor response to angiotensin II in the L-NMMA group was significantly increased as compared with that in the control group, at doses of 50, 100, and 200 ng/kg. The response of the L-NMMA plus L-Arg group did not differ significantly from that of the control group.

Conclusion: Results indicate that the infusion of a nitric oxide synthase inhibitor, at a dose insufficient to produce hypertension, increases the pressor response to angiotensin II.

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