Enhancement of renal prostaglandin E2 and renin release by autoregulatory dilation of preglomerular vessels in dogs.

Renal physiology Pub Date : 1985-01-01 DOI:10.1159/000173050
A Vikse, F Kiil
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引用次数: 13

Abstract

To examine the PGE2 and renin release during autoregulatory dilation of preglomerular vessels, experiments were performed in three groups of anesthetized dogs. By reducing the arterial perfusion pressure from 113 +/- 3 to 78 +/- 3 mm Hg, renin release rose to 20 +/- 50% and PGE2 release to 74 +/- 12% of the maximal values attained at two perfusion pressures below the range of autoregulation. During ureteral occlusion, PGE2 and renin release rose to maximal values already at control blood pressure and remained unaltered as the arterial perfusion pressure was reduced from 124 +/- 7 to 68 +/- 2 mm Hg. Renal blood flow fell in proportion to the perfusion pressure indicating abolished autoregulation. At a perfusion pressure below the range of autoregulation, saline infusion restored sodium excretion and reduced renin release but did not alter PGE2 release. We conclude that PGE2 release is raised by autoregulatory dilation of preglomerular arteries. Prostaglandins enhance renin release when afferent arterioles are dilated. Renin release mediated by a macula densa mechanism is not PGE2 dependent.

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自我调节扩张肾小球前血管对前列腺素E2和肾素释放的促进作用。
为了研究肾小球前血管自我调节扩张过程中PGE2和肾素的释放情况,我们采用三组麻醉犬进行实验。通过将动脉灌注压从113 +/- 3降低到78 +/- 3mmhg,肾素释放上升到20 +/- 50%,PGE2释放上升到74 +/- 12%,这是在两个灌注压低于自动调节范围时达到的最大值。在输尿管阻断期间,PGE2和肾素释放在控制血压下已经上升到最大值,并且在动脉灌注压从124 +/- 7降至68 +/- 2mmhg时保持不变。肾血流量与灌注压成比例下降,表明自动调节已被取消。在低于自身调节范围的灌注压力下,生理盐水输注恢复了钠排泄,减少了肾素释放,但没有改变PGE2的释放。我们得出结论,PGE2的释放通过肾小球前动脉的自我调节扩张而增加。当传入小动脉扩张时,前列腺素促进肾素的释放。由黄斑致密机制介导的肾素释放不依赖于PGE2。
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