Fallgren B, Bjellin L, Edvinsson L
Department of Zoophysiology, University of Lund, Sweden.
Pharmacol Toxicol. 1988 Nov;63(5):375-81. doi: 10.1111/j.1600-0773.1988.tb00971.x.
Adrenoceptor mechanisms in the extrinsic uterine arteries from late pregnant guinea-pigs were characterized pharmacologically and compared with contractile responses of uterine arteries from non-pregnant and oophorectomized control, progesterone and oestrogen treated animals. Pregnancy caused an increase in diameter of the arteries, more pronounced the more distal they were. There was no change in potassium-evoked maximum contractions during pregnancy. Noradrenaline (10 nM to 1 mM), in the presence of cocaine (1 microM) and propranolol (0.1 microM), induced concentration-dependent contractions of the arterial segments, with approximately similar pD2 values. The maximum responses (Emax) were significantly increased during pregnancy and hormone supplementation. Prazosin (10 nM to 1 microM), but not rauwolscine (10 nM to 1 microM), antagonized noradrenaline-evoked contractions of the arteries. Isoprenaline (10 nM to 1 microM), in the presence of prazosin (0.1 microM) and cocaine (1 microM), had no relaxant effect on arteries contracted submaximally by prostaglandin F2a (5 microM). Neither cocaine nor normetanephrine modified noradrenaline-evoked contractions of the uterine artery. The results indicate that guinea-pig uterine vasoconstriction is mediated by alpha 1-adrenoceptors while relaxant beta-adrenoceptor effects, neuronal and extraneuronal uptake mechanisms are of minor importance. The observed increase in Emax may be due either to an increase in the number of alpha 1-adrenoceptors or to an enhanced pharmaco-mechanical coupling, which conceivably is regulated by sex steroids since this response was reproduced in castrated animals by hormone supplementation.
对妊娠晚期豚鼠子宫外动脉的肾上腺素能受体机制进行了药理学表征，并与未妊娠、去卵巢对照、孕激素和雌激素处理动物的子宫动脉收缩反应进行了比较。妊娠导致动脉直径增加，越远端越明显。妊娠期间钾诱发的最大收缩无变化。在可卡因（1μM）和普萘洛尔（0.1μM）存在的情况下，去甲肾上腺素（10 nM至1 mM）诱导动脉段的浓度依赖性收缩，pD2值大致相似。妊娠和激素补充期间最大反应（Emax）显著增加。哌唑嗪（10 nM至1μM）而非萝芙木碱（10 nM至1μM）拮抗去甲肾上腺素诱发的动脉收缩。在哌唑嗪（0.1μM）和可卡因（1μM）存在的情况下，异丙肾上腺素（10 nM至1μM）对前列腺素F2α（5μM）引起的次最大收缩的动脉无舒张作用。可卡因和去甲变肾上腺素均未改变去甲肾上腺素诱发的子宫动脉收缩。结果表明，豚鼠子宫血管收缩由α1-肾上腺素能受体介导，而舒张性β-肾上腺素能受体效应、神经元和非神经元摄取机制的作用较小。观察到的Emax增加可能是由于α1-肾上腺素能受体数量增加或药物-机械偶联增强，鉴于这种反应在去势动物中通过激素补充得以重现，推测其受性类固醇调节。
