Captopril attenuates pressor responses to norepinephrine and vasopressin through depletion of endogenous angiotensin II

Yutaka Imai, Keishi Abe, Masahide Seino, Toshiaki Haruyama, Jiro Tajima, Kaoru Yoshinaga, Hiroshi Sekino

研究成果: Article査読

21 被引用数 (Scopus)

抄録

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 μg/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 < 0.05], 0.2 [p < 0.01]μg/kg · min-1; n = 7) and to vasopressin (p < 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.

本文言語English
ページ(範囲)1537-1539
ページ数3
ジャーナルThe American Journal of Cardiology
49
6
DOI
出版ステータスPublished - 1982 4 21

ASJC Scopus subject areas

  • 循環器および心血管医学

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