Influence of the Renin‐Angiotensin System on the Effect of Prostaglandin Synthesis Inhibitors in the Renal Vasculature
Influence of the Renin‐Angiotensin System on the Effect of Prostaglandin Synthesis Inhibitors in the Renal Vasculature
复制标题
肾素-血管紧张素系统对肾血管中前列腺素合成抑制剂作用的影响
DOI：
10.1161/01.res.36.6.89
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发表时间：
1975
影响因子：
20.1
通讯作者：
B. Zimmerman
中科院分区：
文献类型：
--
作者：
S. Satoh;B. Zimmerman
在基础实验条件下和戊巴比妥麻醉犬肾缺血状态下，测定甲氯芬酯和吲哚美辛对肾血流量和肾血管阻力的影响。用电磁流量计测量肾血流量，用肾动脉导管记录肾动脉压。在基础条件下，动脉内输注吲哚美辛和4 ~ 8吉/ml浓度的甲氯芬酯对肾血、流量和肾血管阻力均无明显影响。在缺血期间（肾血流量减少50%），4 μg/ml任意一种前列腺素合成酶抑制剂引起肾血管阻力显著增加。甲氯芬酯增加肾血管阻力的同时，肾静脉血中前列腺素E降低。在基础和缺血条件下，两种抑制剂均增强了静脉注射血管紧张素II的肾血管收缩反应，这也表明前列腺素的合成受到抑制。血管紧张素拮抗剂l-sar-8- α -血管紧张素II在肾缺血期间以20和40 mg/ml的浓度动脉内输注。随后给予甲氯芬酯仅轻微增加肾血管阻力。上述实验结果提示肾缺血时前列腺素对肾血流的影响大于基础条件下，肾素-血管紧张素系统可能参与激活前列腺素的合成和释放。
The effect of meclofenamate and indomethacin on renal blood flow and renal vascular resistance was determined under basal experimental conditions and during renal ischemia in pentobarbital-anesthetized dogs. Renal blood flow was measured with an electromagnetic flowmeter and renal arterial pressure was recorded from a catheter in the renal artery. Intra-arterial infusion of indomethacin or meclofenamate in concentrations of 4 and 4 to 8 jig/ml, respectively, did not cause any significant change in renal blood, flow or renal vascular resistance under basal conditions. During the period of ischemia (50% reduction in renal blood flow), 4 μg/ml of either prostaglandin synthetase inhibitor caused a marked increase in renal vascular resistance. Prostaglandin E in the renal venous blood was decreased at the time renal vascular resistance was increased by meclofenamate. The renal vasoconstrictor response to angiotensin II injected intravenously was potentiated by both inhibitors under basal as well as ischemic conditions, which also suggested that prostaglandin synthesis was inhibited. The angiotensin antagonist l-sar-8-ala-angioten-sin II was infused intra-arterially in concentrations of 20 and 40 mg/ml during renal ischemia. Subsequent administration of meclofenamate increased renal vascular resistance only slightly. The results of these experiments indicated that renal prostaglandins have more influence on renal blood flow during renal ischemia than under basal conditions, and that the renin-angiotensin system may be involved in activating synthesis and release of prostaglandins during ischemia.