Imai Y, Abe K, Seino M, Haruyama T, Tajima J, Yoshinaga K, Sekino H
Am J Cardiol. 1982 Apr 21;49(6):1537-9. doi: 10.1016/0002-9149(82)90381-2.
The influence of captopril on pressor responses to exogenously administered vasopressor substances was investigated in normal subjects. Norepinephrine (0.05, 0.1 and 0.2 micrograms/kg . min -1; n = 5), angiotensin II (5, 10 and 20 ng/kg . min -1; n = 5) and vasopressin (2 mU/kg . min -1; n = 5) were infused each for 10 minutes; each infusion was repeated twice. Captopril (50 mg orally) significantly attenuated the pressor response to norepinephrine (0.1 [p less than 0.05], 0.2 [p less than 0.01] micrograms/kg . min -1; n = 7) and to vasopressin (p less than 0.01, n = 5), but not to angiotensin II; these responses were reproducible. Attenuation of the pressor responses to norepinephrine did not occur when a subpressor dose of angiotensin II (ng/kg . min-1) was infused in addition to captopril (n = 5). Infusion of a subpressor dose of bradykinin (0.1 ng/kg . min-1) had no influence on the pressor responses to norepinephrine (n = 5). In the five subjects treated with indomethacin (225 mg/54 hours) captopril still attenuated the pressor responses to norepinephrine. These results suggest that the attenuation by captopril of the pressor responses to norepinephrine and vasopressin might have been due to reduction of endogenous angiotensin II.
在正常受试者中研究了卡托普利对外源性给予的血管升压物质升压反应的影响。分别以0.05、0.1和0.2微克/千克·分钟-1（n = 5）的剂量输注去甲肾上腺素10分钟；每种输注重复两次。以5、10和20纳克/千克·分钟-1（n = 5）的剂量输注血管紧张素II 10分钟；每种输注重复两次。以2毫单位/千克·分钟-1（n = 5）的剂量输注血管加压素10分钟；每种输注重复两次。口服卡托普利（50毫克）显著减弱了对去甲肾上腺素（0.1 [p < 0.05]、0.2 [p < 0.01]微克/千克·分钟-1；n = 7）和血管加压素（p < 0.01，n = 5）的升压反应，但对血管紧张素II没有影响；这些反应是可重复的。当除卡托普利外还输注低于升压剂量的血管紧张素II（纳克/千克·分钟-1）时，对去甲肾上腺素的升压反应减弱未出现（n = 5）。输注低于升压剂量的缓激肽（0.1纳克/千克·分钟-1）对去甲肾上腺素的升压反应没有影响（n = 5）。在接受吲哚美辛（225毫克/54小时）治疗的5名受试者中，卡托普利仍然减弱了对去甲肾上腺素的升压反应。这些结果表明，卡托普利对去甲肾上腺素和血管加压素升压反应的减弱可能是由于内源性血管紧张素II的减少。
