Chaud M A, Franchi A M, Gonzalez E T, Gimeno M F, Gimeno A L
Prostaglandins Leukot Med. 1986 May;22(2):201-10. doi: 10.1016/0262-1746(86)90089-2.
The rat uterus generates and releases prostaglandins (PGs) of the series 2 as well as PGs of the series 1. The main purposes of the present study are to compare the effects of norepinephrine (NE) on the production and outputs of PGE1, PGE2 and PGF2 alpha by the uterus isolated from ovariectomized rats, treated or not with 17-beta-estradiol and to explore also, whether the effects of NE on PG synthesis are mediated through alpha, beta or both types of adrenoreceptors. Segments of control uterine horns obtained from ovariectomized rats generated and released into the incubating solution, equal amounts of PGE1, PGE2 and PGF2 alpha and propranolol (10(-6) M) or phentolamine (10(-6) M) failed to alter this basal production of PGs. Norepinephrine (3 X 10(-6) M) significantly depressed the outputs of PGE1 and PGF2 alpha but enhanced, also significantly, the release of PGE2. In the presence of the beta-adrenoreceptor blocker, propranolol, the reduction induced by NE on the output of PGE1 was not altered, but the stimulatory influence of NE on the release of PGE2 as well as the depression on the output of PGF2 alpha, were abolished. On the other hand the diminution evoked by NE on the release of PGF1 and PGF2 alpha as well as the increment induced on PGE2 output, were inhibited by the presence of phentolamine in the incubating solution. Uterine horns from ovariectomized rats treated with 17-beta-estradiol released into the incubating solution significantly more PGF2 alpha than PGE1 or PGE2. NE, either alone of in the presence of alpha 0 or beta-adrenoceptor blockers, did not modify this pattern of PG production. A possible mechanism(s) of action for NE on PG synthesis is discussed.
大鼠子宫能生成并释放2系列前列腺素（PGs）以及1系列PGs。本研究的主要目的是比较去甲肾上腺素（NE）对取自去卵巢大鼠且经或未经17-β-雌二醇处理的子宫中PGE1、PGE2和PGF2α的生成及释放的影响，同时探究NE对PG合成的作用是否通过α、β或两种类型的肾上腺素能受体介导。取自去卵巢大鼠的对照子宫角段生成PGs并释放到培养液中，PGE1、PGE2和PGF2α的量相等，普萘洛尔（10⁻⁶ M）或酚妥拉明（10⁻⁶ M）未能改变PGs的这种基础生成。去甲肾上腺素（3×10⁻⁶ M）显著降低PGE1和PGF2α的释放，但也显著增强PGE2的释放。在β-肾上腺素能受体阻滞剂普萘洛尔存在的情况下，NE对PGE1释放的降低作用未改变，但NE对PGE2释放的刺激作用以及对PGF2α释放的抑制作用均被消除。另一方面，培养液中酚妥拉明的存在抑制了NE对PGF1和PGF2α释放的降低作用以及对PGE2释放的增强作用。用17-β-雌二醇处理的去卵巢大鼠的子宫角释放到培养液中的PGF2α显著多于PGE1或PGE2。单独使用NE或在存在α或β肾上腺素能受体阻滞剂的情况下，NE均未改变这种PG生成模式。本文讨论了NE对PG合成的可能作用机制。
