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实验性糖尿病中肾脏血管对花生四烯酸的反应性

Renal vascular responsiveness to arachidonic acid in experimental diabetes.

作者信息

Quilley J, McGiff J C

机构信息

Dept. Pharmacology, New York Medical College, Valhalla 10595.

出版信息

Br J Pharmacol. 1990 Jun;100(2):336-40. doi: 10.1111/j.1476-5381.1990.tb15805.x.

Abstract
  1. Isolated perfused kidneys from diabetic rats (duration 4-6 and 20-24 weeks) were more sensitive to the vasoconstrictor effects of arachidonic acid than kidneys from age-matched control rats. Sensitivity diminished with age in both control and diabetic groups. 2. The enhanced vasoconstrictor effect of arachidonic acid in diabetic rat kidneys was associated with increased conversion to prostaglandins. 3. The renal vasoconstrictor response to arachidonic acid in both groups was reduced by thromboxane A2/prostaglandin H2 receptor antagonism but not by inhibition of thromboxane synthase. 4. Diabetic rat kidneys were also more sensitive to the vasoconstrictor effects of the endoperoxide analogue, U46619, while vasoconstrictor responses to phenylephrine were not markedly different from those of control rat kidneys. 5. In conclusion, prostaglandin endoperoxides appear to mediate arachidonic acid-induced vasoconstriction in diabetic and control rat kidneys. The enhanced renal vasoconstrictor response to arachidonic acid in diabetic rats results from increased sensitivity to endoperoxides and increased formation of endoperoxides from arachidonic acid.
摘要
  1. 来自糖尿病大鼠(病程4 - 6周和20 - 24周)的离体灌注肾脏对花生四烯酸的血管收缩作用比年龄匹配的对照大鼠的肾脏更敏感。在对照组和糖尿病组中,敏感性均随年龄降低。2. 糖尿病大鼠肾脏中花生四烯酸增强的血管收缩作用与向前列腺素的转化增加有关。3. 两组对花生四烯酸的肾血管收缩反应通过血栓素A2/前列腺素H2受体拮抗作用而降低,但不受血栓素合酶抑制的影响。4. 糖尿病大鼠肾脏对内过氧化物类似物U46619的血管收缩作用也更敏感,而对去氧肾上腺素的血管收缩反应与对照大鼠肾脏的反应无明显差异。5. 总之,前列腺素内过氧化物似乎介导了糖尿病和对照大鼠肾脏中花生四烯酸诱导的血管收缩。糖尿病大鼠对花生四烯酸增强的肾血管收缩反应是由于对内过氧化物的敏感性增加以及花生四烯酸向内过氧化物的形成增加。

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Influence of streptozotocin diabetes on myocardial lipids and prostaglandin release by the rat heart.
Biochem Med. 1983 Aug;30(1):19-33. doi: 10.1016/0006-2944(83)90004-2.
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