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Local inhibition of converting enzyme and vascular responses to angiotensin and bradykinin in the human forearm.

机译:人类前臂中转化酶和血管对血管紧张素和缓激肽的反应的局部抑制。

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摘要

1. The function of angiotensin converting enzyme was investigated in twenty-four healthy men. Forearm blood flow was measured under basal conditions and during administration of enalaprilat (a converting enzyme inhibitor) and/or peptide substrates of converting enzyme into the left brachial artery. Blood flow was compared in the two arms. 2. Enalaprilat had no effect on basal blood flow. The concentration of enalaprilat in venous blood from the control arm was low, and plasma renin activity was not increased, indicating that systemic inhibition of converting enzyme did not occur. 3. Effects of angiotensin and of bradykinin, administered intra-arterially, were limited to the infused arm. Enalaprilat (13 nmol min-1) inhibited converting enzyme in the infused arm, in which it caused approximately a 100-fold reduction in sensitivity to angiotensin I, while having no effect on the vasoconstriction caused by angiotensin II. Enalaprilat increased vasodilatation caused by bradykinin. 4. Aspirin, an inhibitor of cyclo-oxygenase, did not inhibit vasodilatation caused by bradykinin whether infused alone or with enalaprilat, indicating that these responses are not mediated by prostaglandins. 5. We conclude that under basal conditions neither conversion of angiotensin I to angiotensin II nor degradation of bradykinin determines resistance vessel tone in the human forearm. Converting enzyme may affect vascular tone in situations in which intravascular concentrations of peptides are increased over those present under basal conditions.
机译:1.在24名健康男性中研究了血管紧张素转化酶的功能。在基础条件下以及在服用依那普利拉(一种转化酶抑制剂)和/或将酶转化为左臂动脉的肽底物期间,测量前臂的血流量。比较两组的血流量。 2.依那普利拉对基础血流没有影响。来自对照臂的静脉血中的依那普利拉浓度低,血浆肾素活性没有增加,表明未发生全身抑制转化酶的作用。 3.动脉内给药的血管紧张素和缓激肽的作用仅限于输注的手臂。依那普利拉(13 nmol min-1)抑制了输注臂中的转化酶,在该酶中,它对血管紧张素I的敏感性降低了约100倍,而对血管紧张素II引起的血管收缩没有影响。依那普利拉增加缓激肽引起的血管舒张。 4.阿司匹林,一种环加氧酶的抑制剂,无论是单独注入还是与依那普利拉合用,均未抑制由缓激肽引起的血管舒张,表明这些反应不是由前列腺素介导的。 5.我们得出结论,在基础条件下,血管紧张素I转化为血管紧张素II或缓激肽的降解都不会决定人前臂的抵抗血管张力。在肽的血管内浓度高于在基础条件下存在的肽浓度的情况下,转化酶可能会影响血管紧张度。

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