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首页> 外文期刊>Japanese Journal of Pharmacology >The Functional Ratio of Chymase and Angiotensin Converting Enzyme in Angiotensin I-Induced Vascular Contraction in Monkeys, Dogs and Rats
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The Functional Ratio of Chymase and Angiotensin Converting Enzyme in Angiotensin I-Induced Vascular Contraction in Monkeys, Dogs and Rats

机译:猴,狗和大鼠中血管紧张素I引起的血管收缩中胸苷酶和血管紧张素转化酶的功能比

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References(27) Cited-By(16) Recently, a chymase-dependent angiotensin (Ang) II-forming pathway was found in human cardiovascular tissues, and the significance of this pathway in the pathogenesis of some cardiovascular diseases was suggested. The present study examined the ratio of angiotensin converting enzyme (ACE) to chymase-dependent Ang II formation in various isolated vessels from monkeys, dogs and rats. In all of the examined vessels, the addition of KCl at a concentration of 50 mM could induce a maximal contraction. Except for monkey coronary artery and rat renal and femoral artery, the addition of Ang I could induce transitory contractions, whereas the force of contractions in these vessels was quite different. The sensitivity to Ang II in these vessels was similar to that for Ang I. In monkey gastroepiploic and mesenteric arteries, about 70% of the Ang I-induced contraction was suppressed by chymase inhibition, while it was suppressed about 50% in monkey renal, femoral and carotid arteries. In dog renal arteries, about 65% of the Ang I-induced contraction was suppressed by chymase inhibition, while it was suppressed by about 30% in other dog arteries. In contrast, in all rat arteries, Ang I-induced contractions were completely suppressed by treatment with ACE inhibitor alone. We concluded that regional differences in the response to Ang I exist in vascular tissues, and the ratio of ACE- to chymase-dependent Ang II formation is different in the various vessels.
机译:参考文献(27)被By(16)引用最近,在人的心血管组织中发现了一种糜酶依赖性血管紧张素(Ang)II形成途径,该途径在某些心血管疾病的发病机理中具有重要意义。本研究检查了在来自猴子,狗和大鼠的各种分离的血管中血管紧张素转化酶(ACE)与糜酶依赖性Ang II形成的比率。在所有检查过的血管中,添加浓度为50 mM的KCl可能引起最大收缩。除猴冠状动脉和大鼠肾及股动脉外,Ang I的添加可引起短暂性收缩,而这些血管中的收缩力却大不相同。这些血管对Ang II的敏感性与Ang I相似。在猴胃上皮和肠系膜动脉中,糜蛋白酶抑制可抑制约Ang I诱导的收缩的70%,而在猴肾中可抑制约50%。股动脉和颈动脉。在狗的肾动脉中,约有65%的Ang I诱导的收缩被糜蛋白酶抑制所抑制,而在其他的狗动脉中则被抑制了约30%。相反,在所有大鼠动脉中,仅用ACE抑制剂治疗均可完全抑制Ang I诱导的收缩。我们得出的结论是,血管组织中存在着对Ang I反应的区域差异,并且在各种血管中ACE依赖于糜酶的Ang II形成的比率也不同。

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