BRADYKININ VASCULAR INFLUENCE AND ACE INHIBITION

激肽释放酶-激肽系统的作用及其与血管紧张素转换酶的相互作用 肾素-血管紧张素系统在肾脏中的作用及其作用 血管紧张素转换酶(ACE)抑制剂的种类还不是很清楚。 通过使用共同阻断激肽释放酶-激肽系统的药物 对于血管紧张素II(ALL)拮抗剂，我们将确定 激动素对血压(BP)、肾血流量(RBF)、肾小球滤过率(GFR)、尿流量和 麻醉兔体内钠、钾排泄。这些参数 在基础条件下和血管紧张素转换酶抑制期间测定。激活素 对比限钠、限钠、限钠条件下的影响。 补充剂和三种形式的高血压。无论是急症患者还是 血管紧张素转换酶抑制剂的长期应用将在这些不同的 条件。它被假设在两个物体之间存在相互作用 肾素-血管紧张素系统和激肽释放酶-激动素系统。通过分析 激肽和AH的血管参与当这些系统被激活时， 我们将通过这些获得有关BP和血流调节的信息 多肽激素。将通过电流计监测BP和RBF， 测定血浆肾素活性及缓激肽拮抗剂的作用， DAG(Hyp3，DPhe7)缓激肽(NPY 567)和新的非肽ALL拮抗剂 (DUP 753)或沙拉菌素对血压、RBF、肾功能和 对血管紧张素转换酶抑制剂的反应。在确定激动素的作用之后 这些参数在体内，更详细地研究了调节因素 肾脏激动素的释放和代谢将继续进行。一种新型缓释片的研制 本实验室建立的兔肾内动脉网络将 被利用。首先，测定活性激肽释放酶和前激肽释放酶。 在肾内动脉的微体部分，由钠限制和 补充动物，以及来自低和高肾素高血压患者。第二， 动脉网络将被灌流和超融合以允许确定 从血管管腔和血管腔部位释放激动素。怎么都是 拮抗剂、ACE抑制剂、β-肾上腺素能受体激动剂和拮抗剂，以及 激动素代谢抑制剂影响肾动脉激动素的释放 将有助于更好地理解激肽在正常肾脏中的作用 以及受高血压影响的人。

The role of the kallikrein-kinin system and its interaction with the renin-angiotensin system in the kidney and its contribution to the effect of angiotensin converting enzyme (ACE) inhibitors is not well understood. Through the use of agents that block the kallikrein-kinin system together with angiotensin II (All) antagonists, we will determine the influence of kinins on blood pressure (BP), renal blood flow (RBF), GFR, urine flow, and sodium and potassium excretion in the anesthetized rabbit. These parameters will be measured under basal conditions and during inhibition of ACE. Kinin influence will be contrasted under conditions of sodium restriction, sodium supplementation and in three forms of hypertension. Both the acute and chronic application of ACE inhibitors will be examined under these various conditions. It is hypothesized that there is an interaction between the renin-angiotensin system and the kallikrein-kinin system. By analyzing the vascular participation of kinins and AH when these systems are activated, we will gain information about BP and blood flow regulation by these peptide hormones. BP and RBF, by electroflowmetry, will be monitored, plasma renin activity determined, and the effects of bradykinin antagonist, DArg(Hyp3,DPhe7) bradykinin (NPY 567) and new nonpeptide All antagonist (DUP 753) or saralasin determined on BP, RBF, renal function and the response to an ACE inhibitor. After establishing the role of kinins on these parameters In Vivo, more detailed studies on the factors regulating renal kinin release and metabolism will be pursued. A novel preparation of the rabbit intrarenal arterial network developed in this laboratory will be utilized. First, active kallikrein and prekallikrein will be determined in a microsomal fraction of intrarenal arteries from sodium restricted and supplemented animals, and from low and high renin hypertensives. Secondly, the arterial network will be perfused and superfused to allow determination of kinin release from the vascular lumenal and ablumen sites. How AII antagonists, ACE inhibitor, beta-adrenoceptor agonist and antagonist, and inhibitors of kinin metabolism affect kinin release from the renal arteries will provide a better understanding of the kinin role in the normal kidney and that affected by hypertension.