Renal vascular responses and eicosanoid release in diabetic rats.
Renal vascular responses and eicosanoid release in diabetic rats.
复制标题
糖尿病大鼠的肾血管反应和类二十烷酸释放。
DOI：
10.1152/ajprenal.1989.257.5.f762
复制
发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Quilley,J
中科院分区：
文献类型：
--
作者：
Sarubbi,D;McGiff,JC;Quilley,J
在用链脲佐菌素（STZ）诱导雄性Wistar大鼠糖尿病后5天、2周和8-12周，测定了精氨酸加压素（AVP; 1 - 10 ng）和血管紧张素II（ANG II; 1-10 ng）对肾灌注压和类花生酸释放的影响。在诱导糖尿病后2周和8-12周，肾脏对AVP和ANG II的灌注压反应降低，但在5天内没有降低。然而，AVP和血管紧张素II刺激的释放到肾静脉流出物中的肾上腺素在所有测试时间都被抑制。用吲哚美辛抑制环氧合酶对ANG II和AVP的灌注压反应没有显著影响。同样，将灌注液葡萄糖水平提高至400 mg/dl或向灌注液中加入胰岛素（180 microU/ml）也未能改变对ANG II的反应。与此相反，给糖尿病大鼠肾脏施用0.3微克花生四烯酸（AA）（接近对照大鼠肾脏阈值的剂量）导致灌注压显著增加。与糖尿病大鼠AA的肾灌注压增加相关的是前列腺素E2和前列环素的肾静脉流出量与对照组相比显著增加。这些数据表明，糖尿病大鼠中AA的肾脱酰-再酰化缺陷与环氧合酶活性增加相关。
Changes in renal perfusion pressure and eicosanoid release in response to arginine vasopressin (AVP; 1-10 ng) and angiotensin II (ANG II; 1-10 ng) were determined 5 days, 2 wk, and 8-12 wk after the induction of diabetes with streptozotocin (STZ) in male Wistar rats. Renal perfusion pressure responses to AVP and ANG II were reduced at 2 and 8-12 wk, but not at 5 days, after the induction of diabetes. However, AVP- and ANG II-stimulated release of prostaglandins into the renal venous effluent was depressed at all times tested. Inhibition of cyclooxygenase with indomethacin did not significantly influence the perfusion pressure responses to ANG II and AVP. Likewise, raising perfusate glucose levels to 400 mg/dl or adding insulin (180 microU/ml) to the perfusate failed to modify responses to ANG II. In contrast, administration of 0.3 microgram arachidonic acid (AA), a dose approaching threshold in control rat kidneys, to the kidney of the diabetic rat resulted in a marked increase in perfusion pressure. Associated with the increase in renal perfusion pressure to AA in the diabetic rat were significant increases in renal venous efflux of prostaglandin E2 and prostacyclin compared with control. These data suggest a defect in renal deacylation-reacylation of AA associated with an increase in cyclooxygenase activity in the diabetic rat.