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首页> 外文期刊>Clinical and experimental pharmacology & physiology >ARGINASE II AUGMENTS ADRENERGIC VASOCONSTRICTION VIA A BETA-ADRENERGIC, NITRIC OXIDE INDEPENDENT PATHWAY: EVIDENCE FROM THE ARGINASE H KNOCKOUT MOUSE
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ARGINASE II AUGMENTS ADRENERGIC VASOCONSTRICTION VIA A BETA-ADRENERGIC, NITRIC OXIDE INDEPENDENT PATHWAY: EVIDENCE FROM THE ARGINASE H KNOCKOUT MOUSE

机译:精氨酸酶II通过β-肾上腺素,一氧化氮独立途径增强肾上腺血管狭窄:来自精氨酸酶H敲除小鼠的证据

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摘要

Background: Arginase, which shares the common substrate L-argjnine with nitric oxide synthase (NOS), is upregulated in hypertension and other states of endothelial dysfunction4'5. We have demonstrated that non-specific arginase inhibition prevents tolerance to acetylcholine-elicited relaxation in the rat isolated aorta. There are 2 isoforms of arginase, type I and II. In the current study we investigate the role of arginase isoform type II on vascular responses as a potential mechanism by which arginase influences blood pressure
机译:背景:精氨酸酶与一氧化氮合酶(NOS)具有共同的底物L-精氨酸,在高血压和其他内皮功能障碍状态下均被上调4'5。我们已经证明,非特异性精氨酸酶抑制作用阻止了大鼠离体主动脉中对乙酰胆碱引起的松弛的耐受。精氨酸酶有两种同工型,I型和II型。在本研究中,我们调查了II型精氨酸酶同工型在血管反应中的作用,这是精氨酸酶影响血压的潜在机制。

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