Effect of prostaglandin endoperoxide analogue on canine renal function, hemodynamics and renin release.
Effect of prostaglandin endoperoxide analogue on canine renal function, hemodynamics and renin release.
复制标题
前列腺素内过氧化物类似物对犬肾功能、血流动力学和肾素释放的影响。
DOI：
10.1016/0014-2999(79)90129-8
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发表时间：
1979
影响因子：
5
通讯作者：
A. Nies
中科院分区：
文献类型：
--
作者：
J. Gerber;E. Ellis;J. Hollified;A. Nies
我们研究了前列腺素内过氧化物（EPA）的稳定的环醚类似物对犬肾功能，血流动力学和肾素释放的影响。将EPA输注到一个肾动脉中以剂量依赖性方式降低肾血流量。在10 - 7 g/kg/min的剂量下，肾血流量从基线384 ml/min/100 g降至267 ml/min/100 g。酚妥拉明和沙拉新没有改变这种血流减少，但经吲哚美辛预先治疗后增强。尿流量、肾小球滤过率、钠和钾排泄均以剂量依赖性方式降低;然而，钠排泄分数和游离水清除率均未显示任何显著变化，使得EPA不太可能产生直接的肾小管效应。EPA引起了肾素释放的显着增加，这是完全阻断了先前的治疗与吲哚美辛。我们得出结论，EPA是一种有效的肾血管收缩剂，这种血管收缩剂是负责观察到的肾功能变化。肾素释放不是EPA的直接作用，但可能是内源性产生的前列腺素的继发作用。由于EPA模拟天然前列腺素内过氧化物对平滑肌的体外作用，因此体内前列腺素内过氧化物诱导的血管收缩可能调节其血管舒张产物前列腺素E2和I2的作用。
We studied the effect of a stable, cyclic ether analogue of prostaglandin endoperoxide (EPA) on canine renal function, hemodynamics, and renin release. Infusion of EPA into one renal artery decreased renal blood flow in a dose dependent manner. At a dose of 10−7g/kg/min the renal blood flow decreased from a baseline of 384 to 267 ml/min/100 g. This flow decrease was unaltered by phentolamine and saralasin, but was potentiated by prior treatment with indomethacin. Urine flow, glomerular filtration rate, sodium, and potassium excretion all decreased in a dose dependent manner; however, neither fractional excretion of sodium nor free water clearance showed any significant change, making direct tubular effects of EPA unlikely. EPA caused a significant increase in renin release that was completely blocked by prior treatment with indomethacin. We conclude that EPA is a potent renal vasoconstriction and that this vasoconstrictor is responsible for the renal functional changes observed. Renin release is not a direct effect of EPA but probably is secondary to an endogenously generated prostaglandin. Since EPA mimics the effects of natural prostaglandin endoperoxides on smooth muscle in vitro, it is possible that prostaglandin endoperoxide-induced vasoconstriction in vivo modulates the effects of their vasodilatory products, prostaglandin E2and I2.