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血管紧张素II和前列腺素对直小血管血流的控制

Angiotensin II and prostaglandins in control of vasa recta blood flow.

作者信息

Cupples W A, Sakai T, Marsh D J

机构信息

Department of Physiology and Biophysics, University of Southern California, Los Angeles 90033.

出版信息

Am J Physiol. 1988 Mar;254(3 Pt 2):F417-24. doi: 10.1152/ajprenal.1988.254.3.F417.

Abstract

Angiotensin II has been implicated in the regulation of medullary blood flow and is known to interact with prostaglandins at sites within the kidney. Therefore the role of angiotensin in control of vasa recta blood flow was studied in antidiuretic, Munich-Wistar rats. We also tested the hypothesis that prostaglandins act to modulate the effect of angiotensin. Total renal blood flow was measured by an electromagnetic flow probe, vasa recta blood flow by a dual-slit method. Captopril was used to confirm that angiotensin blockade increased renal blood flow (by 15 +/- 4%). Captopril and saralasin were used to show that angiotensin blockade increased vasa recta blood flow (by 23 +/- 9 and 14 +/- 7%, respectively). The results demonstrate a tonic constrictor effect of angiotensin in the renal medulla. Exogenous angiotensin II, delivered intravenously, failed to mimic the effect of endogenous angiotensin. Indomethacin did not alter blood pressure or renal blood flow but did reduce vasa recta blood flow by 20 +/- 3%, suggesting that prostaglandins act preferentially on the medullary circulation. Nor did it alter the response of blood pressure, of renal blood flow, or of vasa recta blood flow to captopril. Moreover, prior angiotensin blockade with either captopril or saralasin enhanced the medullary vasoconstrictor effect of indomethacin (P less than 0.05). These results are not consistent with the hypothesis that prostaglandins act primarily as angiotensin modulators. They suggest that the medullary interaction between angiotensin and prostaglandins differs from that in the cortex.

摘要

血管紧张素II与髓质血流调节有关,并且已知它在肾脏内的一些部位与前列腺素相互作用。因此,在抗利尿的慕尼黑-威斯塔大鼠中研究了血管紧张素在控制直小血管血流中的作用。我们还检验了前列腺素起到调节血管紧张素作用的假说。用电磁血流探头测量总肾血流量,用双缝法测量直小血管血流量。使用卡托普利来证实血管紧张素阻断可增加肾血流量(增加15±4%)。使用卡托普利和沙拉新表明血管紧张素阻断可增加直小血管血流量(分别增加23±9%和14±7%)。结果表明血管紧张素在肾髓质具有紧张性收缩作用。静脉注射外源性血管紧张素II无法模拟内源性血管紧张素的作用。吲哚美辛未改变血压或肾血流量,但使直小血管血流量减少了20±3%,这表明前列腺素优先作用于髓质循环。它也未改变血压、肾血流量或直小血管血流量对卡托普利的反应。此外,预先用卡托普利或沙拉新进行血管紧张素阻断可增强吲哚美辛的髓质血管收缩作用(P<0.05)。这些结果与前列腺素主要作为血管紧张素调节剂的假说不一致。它们表明血管紧张素与前列腺素在髓质中的相互作用不同于在皮质中的相互作用。

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