Feedback pressure-flow responses in normal and angiotensin-prostaglandin-blocked rats.
Feedback pressure-flow responses in normal and angiotensin-prostaglandin-blocked rats.
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正常和血管紧张素前列腺素阻断大鼠的反馈压力-流量反应。
DOI：
10.1152/ajprenal.1984.247.6.f925
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Blantz,RC
中科院分区：
文献类型：
--
作者：
Persson,AE;Gushwa,LC;Blantz,RC
我们研究了直接和间接（停流）测量肾小球毛细血管静水压力（PGC）和单个肾单位肾小球滤过率（SNGFR）的反应，以增加在晚期近端肾小管流速在缺水大鼠和大鼠，其中血管紧张素II（ANG II）和前列腺素的产生减少了3- 5天的预处理转换酶抑制剂（MK-421）和甲氨蝶呤。在对照组大鼠中，当在未阻塞的小管中向晚期近端血流增加25 nl/min时，PGC（48 +/- 2 mmHg）降低9 +/- 1 mmHg，而在蜡阻塞的小管中，当晚期近端灌注速率从0增加到40 nl/min时，PGC降低9 +/-1 mmHg。PGC的转折点或半最大反应是在灌注速率为23 +/- 2 nl/min时。停流估计的PGC（47 +/- 1 mmHg =对照）反应几乎相同。在对照大鼠中，随着灌注增加，SNGFR从30 +/- 1降至21 +/- 1 nl/min。在ANG II-前列腺素阻断大鼠中，PGC和停流压力反应被完全消除，但SNGFR反应持续存在（36.2至28.0 nl/min），但程度较轻。直接和间接PGC均随未治疗大鼠晚期近端流速的增加而降低。ANG II前列腺素阻断大鼠的研究表明，肾小管肾小球反馈SNGFR反应可以发生在PGC没有变化，可能通过传入和传出小动脉阻力的平行变化。
We have examined the response of directly and indirectly (stop-flow) measured glomerular capillary hydrostatic pressure (PGC) and single nephron glomerular filtration rate (SNGFR) to increases in late proximal tubular flow rate in hydropenic rats and rats in which angiotensin II (ANG II) and prostaglandin generation was reduced by 3- to 5-day pretreatment with converting enzyme inhibitor (MK-421) and meclofenamate. In control rats, PGC (48 +/- 2 mmHg) decreased 9 +/- 1 mmHg when 25 nl/min was added to late proximal flow in unobstructed tubules, and PGC decreased 9 +/- 1 mmHg when late proximal perfusion rate was increased from 0 to 40 nl/min, incrementally, in wax-blocked tubules. The turning point or half-maximal response for PGC was at perfusion rates of 23 +/- 2 nl/min. Stop-flow estimated PGC (47 +/- 1 mmHg = control) responses were nearly identical. SNGFR decreased from 30 +/- 1 to 21 +/- 1 nl/min with increased perfusion in control rats. In ANG II-prostaglandin-blocked rats, PGC and stop-flow pressure responses were completely eliminated, yet SNGFR response persisted (36.2 to 28.0 nl/min) but to a somewhat lesser extent. Both direct and indirect PGC decrease with increases in late proximal flow rate in untreated rats. Studies in ANG II-prostaglandin-blocked rats suggest that tubuloglomerular feedback SNGFR responses can occur without changes in PGC, possibly via parallel changes in afferent and efferent arteriolar resistances.