Enhanced Renal Prostaglandin Production in the Dog: II. EFFECTS ON INTRARENAL HEMODYNAMICS
Enhanced Renal Prostaglandin Production in the Dog: II. EFFECTS ON INTRARENAL HEMODYNAMICS
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增强狗肾前列腺素的产生：II。
DOI：
10.1161/01.res.36.1.204
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发表时间：
1975
影响因子：
20.1
通讯作者：
A. Nies
中科院分区：
文献类型：
--
作者：
L. Chang;J. Spławiński;J. Oates;A. Nies
通过将花生四烯酸钠（肾胰高血糖素的前体）输注到狗的一个肾动脉中来评估肾胰高血糖素的增强的内源性产生对肾皮质中血流分布的影响。将花生四烯酸（3 × 10−6 g/kg min−1和10−5 g/kg min−1）产生的变化与向一条肾动脉输注前列腺素（PG）E2（10−7 g/kg min−1）和PGF 2 α（3 × 10−7 g/kg min−1）产生的变化进行比较。放射性微球技术测定肾血流分布。花生四烯酸钠引起内皮质区血流量增加，而皮质最外侧四分之一肾单位血流量无变化。PGE 2增加了所有皮质区的血流量，PGF 2 α对血流量无影响。由于动脉血压没有变化，血管阻力的变化与血流的变化是相互的。因此，输注花生四烯酸后，内皮层区域的血管阻力下降，而外皮层区域的血管阻力没有下降，输注PGE 2后，所有皮层区域的血管阻力都下降;输注PGF 2 α后，未观察到任何变化。这些数据表明，前列腺素在肾脏内源性形成的影响血管阻力，只有内皮质肾单位的数据，从而支持这一假设，即肾肾上腺素是肾血流自动调节的介质之一。
The effects of enhanced endogenous production of prostaglandins by the kidney on the distribution of blood flow in the renal cortex were assessed by infusing sodium arachidonate, the precursor of the renal prostaglandins, into one renal artery of the dog. The changes produced with arachidonate (3 × 10−6 g/kg min−1 and 10−5 g/kg min−1) were compared with those produced by infusions of prostaglandin (PG) E2 (10−7 g/kg min−1) and PGF2α (3 × 10−7 g/kg min−1) into one renal artery. Distribution of renal blood flow was measured by the radioactive microsphere technique. Sodium arachidonate caused an increase in blood flow to the inner cortical zones with no change in flow to the nephrons in the outermost quarter of the cortex. PGE2 increased flow to all cortical zones, and PGF2α produced no change in flow. Since arterial blood pressure did not change, changes in vascular resistance were reciprocal to changes in flow. Thus, vascular resistance fell in the inner cortical regions but not in the outer regions, with arachidonate infusions and in all regions of the cortex with PGE2 infusions; no changes were seen with PGF2α infusions. These data indicate that prostaglandin formed endogenously in the kidney affects the vascular resistance of only the inner cortical nephrons; the data thus support the hypothesis that renal prostaglandins are one mediator of renal autoregulation of blood flow.