肾前列腺素合成酶系统的刺激与抑制对体内及体外肾素释放的影响。

Effects of stimulation and inhibition of the renal prostaglandin synthetase system on renin release in vivo and in vitro.

Weber P C, Larsson C, Hamberg M, Anggård E, Corey E J, Samuelsson B

Clin Sci Mol Med Suppl. 1976 Dec;3:271s-274s. doi: 10.1042/cs051271s.

Abstract

The prostaglandin precursor arachidonic acid (C20:4) increases plasma renin activity in the rabbit and rat when it is infused into the renal arteries. 2. The increase in plasma renin activity after C20:4 in rats is not changed by volume expansion. 3. The inhibitor of prostaglandin synthesis indomethacin decreases plasma renin activity in the rabbit. 4. The increase plasma in renin activity after total renal ischaemia is abolished by pretreatment with indomethacin. 5. C20:4 increases dose- and time-dependent renin release from slices of rabbit kidney cortex. 6. Indomethacin or 5,8,11,14-eicosatetraynoic acid pretreatment in vivo, and addition to the incubation medium, reduces basal as well as C20:4-stimulated renin release in vitro. 7. The stimulating effect of C20:4 on renin release is assumed to be caused directly by formation of prostaglandin endoperoxides in the kidney cortex and not by prostaglandins since in vitro a natural prostaglandin endoperoxide (PGG2) and two stable synthetic prostaglandin endoperoxide analogues (EPA I and EPA II) do increase the release of renin, but PGE2 has no effect and PGF2alpha inhibits renin release.

摘要

当将前列腺素前体花生四烯酸（C20:4）注入兔和大鼠的肾动脉时，它会增加血浆肾素活性。2. 大鼠注射C20:4后血浆肾素活性的增加不受血容量扩充的影响。3. 前列腺素合成抑制剂消炎痛可降低兔的血浆肾素活性。4. 消炎痛预处理可消除完全性肾缺血后血浆肾素活性的增加。5. C20:4可使兔肾皮质切片的肾素释放呈剂量和时间依赖性增加。6. 体内用消炎痛或5,8,11,14-二十碳四炔酸预处理，以及在孵育培养基中加入这两种物质，均可降低体外基础状态以及C20:4刺激的肾素释放。7. C20:4对肾素释放的刺激作用被认为是直接由肾皮质中前列腺素内过氧化物的形成引起的，而不是由前列腺素引起的，因为在体外，天然前列腺素内过氧化物（PGG2）和两种稳定的合成前列腺素内过氧化物类似物（EPA I和EPA II）确实会增加肾素的释放，但PGE2没有作用，PGF2α会抑制肾素释放。