Relative contribution of angiotensin II, bradykinin, and prostaglandins to the renal effects of converting enzyme inhibition in rats after chronic myocardial infarction.
Relative contribution of angiotensin II, bradykinin, and prostaglandins to the renal effects of converting enzyme inhibition in rats after chronic myocardial infarction.
复制标题
血管紧张素 II、缓激肽和前列腺素对慢性心肌梗死后大鼠转化酶抑制的肾脏影响的相对贡献。
DOI：
10.1097/00005344-199607000-00024
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发表时间：
1996
影响因子：
3
通讯作者：
Raya,TE
中科院分区：
文献类型：
--
作者：
Deck,CC;Gaballa,MA;Raya,TE
我们希望确定缓激肽 (BK) 和血管舒张前列腺素生物利用度的增强是否有助于心肌梗死 (MI) 后血管紧张素转换酶 (ACE) 抑制的肾血管和钠处理作用。我们研究了冠状动脉结扎后用卡托普利或氯沙坦（每种药物 2 g/L 饮用水）治疗 3 周的大鼠。在连续输注 BK 抑制剂（BKI，0.02 ng/kg/min）和吲哚美辛（1 mg/kg）前后，对清醒大鼠进行血流动力学和肾功能研究。心肌梗塞使滤过分数 (FF) 增加 20%（p<. 004），但不改变肾小球滤过率 (GFR)、尿流量 (UF)、肾血流量 (RBF)、肾血管阻力 (RVR)、尿钠 (UNa) 或钠排泄分数 (FENa)。卡托普利降低 (p< 0.001) 平均动脉压 (MAP) 25%、UF 61%、RVR 65% 和 FENa 75%，并增加 (p< 0.05) GFR 22% 和 RBF 34%。氯沙坦降低 (p< 0.05) MAP 27%、UF 52%、RVR 21% 和 FENa 44%。在卡托普利治疗的 MI 大鼠中，BKI 降低 (p< 0.05) GFR 22% 和 RBF 25%，并增加 (p< 0.05) RVR 32%、UNa 43% 和 FENa 28%，而吲哚美辛降低 (p< 0.05) GFR 24% 并增加 (p< 0.05) UNa 86% 和 FENa 112%。在氯沙坦治疗的 MI 大鼠中，BKI 增加 (p< 0.05) UNa 42% 和 FENa 60%，而吲哚美辛增加 (p< 0.05) UNa 79% 和 FENa 85%。 BK 和前列腺素系统的激活可能在慢性 ACE 抑制期间调节肾功能中发挥重要作用，主要是通过增强血管紧张素 II (AII) 阻断的肾血管舒张作用。
We wished to determine whether enhanced bioavailability of bradykinin (BK) and vasodilatory prostaglandins contribute to renovascular and sodium-handling effects of angiotensin-converting enzyme (ACE) inhibition after myocardial infarction (MI). We studied rats after coronary artery ligation treated for 3 weeks with captopril or losartan (2 g/L drinking water for each agent). Hemodynamic and renal function studies were performed in conscious rats before and after sequential infusion BK inhibitor (BKI, 0.02 ng/kg/min) and indomethacin (1 mg/kg). Myocardial infarction increased filtration fraction (FF) 20%(p<. 004) but did not change glomerular filtration rate (GFR), urine flow (UF), renal blood flow (RBF), renal vascular resistance (RVR), urine sodium (UNa), or fractional excretion of sodium (FENa). Captopril decreased (p< 0.001) mean arterial pressure (MAP) 25%, UF 61%, RVR 65%, and FENa 75% and increased (p< 0.05) GFR 22%, and RBF 34%. Losartan decreased (p< 0.05) MAP 27%, UF 52%, RVR 21%, and FENa 44%. In captopril-treated MI rats, BKI decreased (p< 0.05) GFR 22% and RBF 25% and increased (p< 0.05) RVR 32%, UNa 43%, and FENa 28%, whereas indomethacin decreased (p< 0.05) GFR 24% and increased (p< 0.05) UNa 86% and FENa 112%. In losartan-treated MI rats, BKI increased (p< 0.05) UNa 42% and FENa 60%, whereas indomethacin increased (p< 0.05) UNa 79% and FENa 85%. Activation of the BK and prostaglandin systems may play an important role in regulating renal function during chronic ACE inhibition, primarily by enhancing the renal vasodilatory effects of angiotensin II (AII) blockade.