Sullivan J M, Patrick D R
Prostaglandins. 1981 Oct;22(4):575-85. doi: 10.1016/0090-6980(81)90067-8.
The effect of captopril, furosemide, indomethacin and intake of sodium on the production of PGI2-like material was studied in the rat aorta. Release of PGI2-like material from these vessels was estimated by its ability to inhibit ADP-induced platelet aggregation. Pretreatment with indomethacin (15 mg/kg/day) reduced the capacity of the aorta to release PGI2-like material. Pretreatment with captopril (10 mg/kg/day) had no effect. Intravenous furosemide (60 microgram/ml plasma volume) increased the capacity of the aorta to inhibit by 28% (p less than 0.25). The inhibitory capacity of aorta removed from rats on a low sodium diet did not differ from those on a high sodium diet. We conclude that the action of furosemide in reducing vascular tone may be related to stimulation of PGI2 synthesis in blood vessels whereas the effect of captopril and sodium in reducing vascular tone may involve a mechanism unrelated to PGI2 synthesis or may involve the synthesis of a prostaglandin other than PGI2.
在大鼠主动脉中研究了卡托普利、呋塞米、吲哚美辛及钠摄入对类前列环素（PGI2）物质生成的影响。通过其抑制二磷酸腺苷（ADP）诱导的血小板聚集的能力来评估这些血管中类PGI2物质的释放。用吲哚美辛（15毫克/千克/天）预处理可降低主动脉释放类PGI2物质的能力。用卡托普利（10毫克/千克/天）预处理则无作用。静脉注射呋塞米（60微克/毫升血浆容量）可使主动脉的抑制能力提高28%（p<0.25）。从低钠饮食大鼠身上取下的主动脉的抑制能力与高钠饮食大鼠的主动脉无差异。我们得出结论，呋塞米降低血管张力的作用可能与刺激血管中PGI2的合成有关，而卡托普利和钠降低血管张力的作用可能涉及与PGI2合成无关的机制，或者可能涉及除PGI2之外的其他前列腺素的合成。
