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

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21 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1537-1539
Number of pages3
JournalThe American Journal of Cardiology
Volume49
Issue number6
DOIs
Publication statusPublished - 1982 Apr 21

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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