Han L, Yang H, Shimada T, Hirose T, Koyanagi M, Matsumoto I, Iwasaki K, Aikawa T
Department of Physiology and Orthopedic Surgery, Nagasaki University School of Medicine, Japan.
Life Sci. 1998;62(8):715-26. doi: 10.1016/s0024-3205(97)01170-3.
The effect of SM12502 and CV6209, platelet-activating factor (PAF) receptor antagonists on corticosterone (B) secretion induced by ACTH was examined in the perfused adrenals of CD1 ICR (normal) and CD1 ICR nu/nu (athymic) mice. Bilateral adrenals were perfused in situ with an artificial medium equilibrated by 95% O2 + 5% CO2. Continuous infusion of 10 microM SM12502 or CV6209 inhibited the B response to 100 pg/ml ACTH markedly in normal mice but insignificantly in athymic mice. Infusion of PAF did not significantly affect B secretion in either normal or athymic mice. Administration of 0.1 microM of N-methylcarbamyl PAF, a nonmetabolizable PAF agonist, significantly increased B secretion in normal mice, but not in athymic mice. Infusion of SM12502 significantly depressed the B response to 10 microM forskolin or 1 mM dibutyryl cyclicAMP (cAMP) in normal mice, but not in athymic mice. The results indicate that endogenous PAF and its receptor may play a role in the ACTH-initiated signaling pathway at the phase after responsiveness to cAMP and its receptor may have little function in athymic mice.
在CD1 ICR（正常）和CD1 ICR nu/nu（无胸腺）小鼠的灌注肾上腺中，研究了血小板活化因子（PAF）受体拮抗剂SM12502和CV6209对促肾上腺皮质激素（ACTH）诱导的皮质酮（B）分泌的影响。用95% O2 + 5% CO2平衡的人工培养基对双侧肾上腺进行原位灌注。持续输注10微摩尔SM12502或CV6209可显著抑制正常小鼠对100皮克/毫升ACTH的B反应，但对无胸腺小鼠的抑制作用不明显。输注PAF对正常或无胸腺小鼠的B分泌均无显著影响。给予0.1微摩尔的N-甲基氨基甲酰PAF（一种不可代谢的PAF激动剂）可显著增加正常小鼠的B分泌，但对无胸腺小鼠无此作用。输注SM12502可显著降低正常小鼠对10微摩尔福斯高林或1毫摩尔二丁酰环磷腺苷（cAMP）的B反应，但对无胸腺小鼠无此作用。结果表明，内源性PAF及其受体可能在对cAMP反应后的阶段参与ACTH启动的信号通路，且其受体在无胸腺小鼠中可能作用不大。
