Different responses of cortical and juxtamedullary arterioles to norepinephrine and angiotensin II.

Different responses of cortical and juxtamedullary arterioles to norepinephrine and angiotensin II.
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皮质和近髓小动脉对去甲肾上腺素和血管紧张素 II 的不同反应。

DOI:
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发表时间:
1990
期刊:
Kidney international. Supplement
影响因子:
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通讯作者:
N. Parekh
N. Parekh
中科院分区:
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文献类型:
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作者:
M. Steinhausen;D. Ballantyne;M. Fretschner;J. Hoffend;N. Parekh

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用活体显微技术测定了Inactin麻醉下雌性Wistar大鼠裂肾肾皮质(C)和髓旁(JM)肾小球血流。静脉注射小剂量、等压剂量的去甲肾上腺素(NE)和血管紧张素II (Ang II)分别使C类传入小动脉直径减少-16 +/- 2.4%和-14 +/- 1.9%,而JM类传入小动脉直径仅减少-3.8 +/- 2.7%和-3.8 +/- 1.5%。在NE和Ang II下,C组肾小球血流分别减少-42 +/- 4.9%和-37 +/- 4.0%,而在JM组肾小球血流分别减少-10 +/- 6.2%和-8.6 +/- 2.9%。NE或Ang输注期间灌注压降至输注前值,仅在C型肾小球中显示出自我调节行为。在第二个系列的实验中,局部给药吲哚美辛(2.8 × 10(-5) M)抑制环加氧酶诱导C和JM血管收缩。在局部应用吲哚美辛时,NE和Ang II的影响是可变的,但C和JM血管的不同反应性消失。我们假设在控制条件下,C和JM血管之间NE和Ang II反应性的差异是由高前列腺素含量或敏感性引起的,特别是肾积水的JM血管。
Cortical (C) and juxtamedullary (JM) glomerular blood flow were measured with intravitalmicroscopic techniques in the split hydronephrotic kidney of female Wistar rats under Inactin anesthesia. Intravenous injection of small, equivalent pressor doses of norepinephrine (NE) and angiotensin II (Ang II) reduced the diameter of C afferent arterioles by -16 +/- 2.4% and -14 +/- 1.9%, respectively, whereas that of JM afferent arterioles was reduced by only -3.8 +/- 2.7% and -3.8 +/- 1.5%. Blood flow under NE and Ang II was reduced in C glomeruli by -42 +/- 4.9% and -37 +/- 4.0%, respectively, but in JM glomeruli was reduced by -10 +/- 6.2% and -8.6 +/- 2.9% of control. Perfusion pressure reduction during NE or Ang II infusion to preinfusion values revealed autoregulatory behavior only in C glomeruli. In a second series of experiments cyclooxygenase inhibition by local administration of indomethacin (2.8 x 10(-5) M) induced C and JM vasoconstriction. The effects of NE and Ang II during local application of indomethacin were variable but different responsiveness of C and JM vessels disappeared. We assume that the differences in NE and Ang II responsiveness between C and JM vessels under control conditions are caused by a high prostaglandin content or sensitivity, particularly of JM vessels in the hydronephrotic kidney.