Kondo K, Okuno T, Suzuki H, Handa M, Saruta T
Jpn Heart J. 1981 Jul;22(4):617-25. doi: 10.1536/ihj.22.617.
In the perfused rat mesenteric vascular bed, the effects of captopril and prostaglandin I2 (PGI2) on the vasoconstrictor responses to norepinephrine or potassium chloride were studied. Captopril or PGI2 in the perfusate attenuated the vascular responses to norepinephrine in a dose-related manner, while these substances had no effect on the vascular contractions induced by potassium chloride. In preparations treated with indomethacin, the inhibitory effect of captopril on the vascular response to norepinephrine was similar to that found in the untreated preparations. These results suggest that, although the effects of captopril on the vascular reactivity is similar to that of PGI2, the direct vascular action of captopril is not mediated by the synthesis of prostaglandins in the vascular bed.
在灌注的大鼠肠系膜血管床中,研究了卡托普利和前列腺素I2(PGI2)对去甲肾上腺素或氯化钾引起的血管收缩反应的影响。灌注液中的卡托普利或PGI2以剂量相关的方式减弱了对去甲肾上腺素的血管反应,而这些物质对氯化钾诱导的血管收缩没有影响。在用吲哚美辛处理的制剂中,卡托普利对去甲肾上腺素血管反应的抑制作用与未处理制剂中的相似。这些结果表明,尽管卡托普利对血管反应性的影响与PGI2相似,但卡托普利的直接血管作用不是由血管床中前列腺素的合成介导的。