Publication Detail
The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Effects of the AT1-receptor antagonist eprosartan on the progression of left ventricular dysfunction in dogs with heart failure.
George Suzuki; Takayuki Mishima; Elaine J Tanhehco; Victor G Sharov; Anastassia Todor; Sharad Rostogi; Ramesh C Gupta; Pervaiz A Chaudhry; Petros V Anagnostopoulos; Omar Nass; et al. (Profiled Author: Hani N Sabbah)
Department of Medicine, Division of Cardiovascular Medicine, Henry Ford Heart & Vascular Institute, Detroit, Michigan 48202, U.S.A.
British journal of pharmacology 2003;138(2):301-9.
1. We examined the effects of eprosartan, an AT(1) receptor antagonist, on the progression of left ventricular (LV) dysfunction and remodelling in dogs with heart failure (HF) produced by intracoronary microembolizations (LV ejection fraction, EF 30 to 40%). 2. Dogs were randomized to 3 months of oral therapy with low-dose eprosartan (600 mg once daily, n=8), high-dose eprosartan (1200 mg once daily, n=8), or placebo (n=8). 3. In the placebo group, LV end-diastolic (EDV) and end-systolic (ESV) volumes increased after 3 months (68+/-7 vs 82+/-9 ml, P<0.004, 43+/-1 vs 58+/-7 ml, P<0.003, respectively), and EF decreased (37+/-1 vs 29+/-1%, P<0.001). In dogs treated with low-dose eprosartan, EF, EDV, and ESV remained unchanged over the course of therapy, whereas in dogs treated with high-dose eprosartan, EF increased (38+/-1 vs 42+/-1%, P<0.004) and ESV decreased (41+/-1 vs 37+/-1 ml, P<0.006), Eprosartan also decreased interstitial fibrosis and cardiomyocyte hypertrophy. 4. We conclude that eprosartan prevents progressive LV dysfunction and attenuates progressive LV remodelling in dogs with moderate HF and may be useful in treating patients with chronic HF.
1 Originating Grant
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1.
Sabbah, Hani N
1 April 1994 - 31 December 2003
NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
Total Funding: $ 2,329,997
Scientific Context
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Related Grants
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1.
Wang, Donna H
Renal Angiotensin II Receptor and Sodium Intake
14 August 1998 - 29 February 2008
NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
Total Funding: $ 1,438,625
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2.
Yingst, Douglas R
Mechanisms of Renal Na+ Pump Stimulation by Angiotensin
1 July 2002 - 30 April 2007
NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES
Total Funding: $ 917,845
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3.
Mattoo, Tej K
Tacrolimus and Plasmapheresis in Treatment-Resistant FSGS
30 September 2006 - 31 August 2008
NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES
Total Funding: $ 421,258
Related Publications
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1.
2002Yun-He Liu; Jiang Xu; Xiao-Ping Yang; Fang Yang; Edward Shesely; Oscar A Carretero
Hypertension 2002;39(2 Pt 2):375-81. -
2.
1999M Tanimura; V G Sharov; H Shimoyama; T Mishima; T B Levine; S Goldstein; H N Sabbah
The American journal of physiology 1999;276(4 Pt 2):H1385-92. -
3.
2001X P Yang; Y H Liu; D Mehta; M A Cavasin; E Shesely; J Xu; F Liu; O A Carretero
Circulation research 2001;88(10):1072-9.
Related Topics
Appears in this Publication
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Angiotensin Receptor Antagon...
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Angiotensin II Type 1 Recept...
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Angiotensin-Converting Enzym...
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Ventricular Dysfunction, Lef...
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Related Experts
Author of this Publication
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Internal ExpertsPublications
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