Campos G A, Guerra F A, Israel E J
Arch Biol Med Exp. 1983 Aug;16(1):43-9.
The effect of Angiotensin II (A-II) on 6-keto-prostaglandin F1 (6-keto-PGF1 alpha) and prostaglandin F (PGF) production by the rat uterus was studied using a novel superfusion technique. The method of superfusion used allows prostaglandin synthesis in the myometrium and endometrium to be measured independently while their anatomical relationship is undisturbed. Prostaglandins were measured by radioimmunoassay. In uterine horns from castrated, estrogen treated rats, A-II (10(-6)M) stimulated the production rate of 6-keto-PGF1 alpha in the myometrium nd PGF in the endometrium. Sterile horns and pregnant horns coexisting in the same animals showed different responses when superfused with culture medium containing A-II (10(-6)M). In the sterile horns A-II failed to stimulate prostaglandin synthesis whereas in the pregnant horns there was a significant increase in the production rate of both 6-keto-PGF1 alpha and PGF in the decidua (endometrium) and of 6-keto-PGF1 alpha in the myometrium. Our results suggests that the effect of A-II on prostaglandin synthesis by the rat uterus appears to be dependent of the hormonal milieu of the experimental animal. Estrogen stimulated A-II induced PG synthesis. Progesterone inhibited the synthesis of PGs caused by A-II in non-decidualized uterus but stimulated the release of PG in the decidualized uterus. The apparent differential effect of A-II in stimulating prostaglandin synthesis in the whole uterus indicates that there are different pathways for prostaglandin production in both the endometrium and myometrium.
采用一种新型的灌注技术，研究了血管紧张素II（A-II）对大鼠子宫产生6-酮-前列腺素F1（6-酮-PGF1α）和前列腺素F（PGF）的影响。所采用的灌注方法能够在不干扰子宫肌层和子宫内膜解剖关系的情况下，独立测量它们合成前列腺素的情况。通过放射免疫分析法测定前列腺素。在摘除卵巢并用雌激素处理的大鼠子宫角中，A-II（10⁻⁶M）刺激了子宫肌层中6-酮-PGF1α和子宫内膜中PGF的产生速率。同一动物体内共存的无菌子宫角和妊娠子宫角在灌注含A-II（10⁻⁶M）的培养基时表现出不同的反应。在无菌子宫角中，A-II未能刺激前列腺素合成，而在妊娠子宫角中，蜕膜（子宫内膜）中6-酮-PGF1α和PGF的产生速率以及子宫肌层中6-酮-PGF1α的产生速率均显著增加。我们的结果表明，A-II对大鼠子宫前列腺素合成的影响似乎取决于实验动物的激素环境。雌激素刺激了A-II诱导的PG合成。孕酮在未蜕膜化的子宫中抑制A-II引起的PG合成，但在蜕膜化的子宫中刺激PG释放。A-II在刺激整个子宫前列腺素合成方面明显的差异效应表明，子宫内膜和子宫肌层中前列腺素的产生存在不同途径。
