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Cited by 579

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Angiotensin II-forming pathways in normal and failing human hearts.

Open access
Urata, H, Healy, B, Stewart, R W, Bumpus, F M, Husain, A·1990·Circulation Research

Abstract

Reduced preload and afterload to the heart are important effects of angiotensin converting enzyme (ACE) inhibitors in the treatment of congestive heart failure. However, since angiotensin II (Ang II) directly increases the strength of myocardial contraction, suppression of Ang II formation by ACE inhibitors could potentially reduce the beneficial effects of Ang II on the failing heart. To study how ACE inhibition suppresses cardiac Ang II formation in man, we characterized ACE-dependent and ACE-independent Ang II-forming pathways in eight normal and 24 failing human hearts obtained at cardiac transplantation. Ang II-forming activity in left ventricular (LV) membrane preparations was assessed by measuring the conversion of [125I]angiotensin I (Ang I) to [125I]Ang II. LV [125I]Ang II-forming activity in normal hearts (35.5 +/- 2.7 fmol/min/mg, n = 8) was not different from that in hearts from patients with ischemic cardiomyopathy (25.5 +/- 2.9 fmol/min/mg, n = 9) and was 48% lower (p less than 0.001) in hearts from patients with idiopathic cardiomyopathy (18.5 +/- 1.9 fmol/min/mg, n = 15).(ABSTRACT TRUNCATED AT 250 WORDS)

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Crossref · 10.1161/01.res.66.4.883

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Metadata

Authors
Urata, H., Healy, B., Stewart, R. W., Bumpus, F. M., & Husain, A.
Venue
Circulation Research
Published
1990-04
Volume
66
Issue
4
Pages
883-890
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
OpenAlex
W2171083892
Cited by
579
References
1
FWCI
16.51
Type
journal article
Language
en
Open access
bronze

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