The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index.
Correction of Arterial Structure and Endothelial Dysfunction in Human Essential Hypertension by the Angiotensin Receptor Antagonist Losartan
Abstract
Background —Structural and functional alterations of the vasculature may contribute to complications of hypertension. Because angiotensin II may be pivotal in some of these vascular abnormalities, we tested the hypothesis that the angiotensin type 1 (AT 1 ) receptor antagonist losartan, in contrast to the β-blocker atenolol, would correct resistance artery abnormalities in patients with essential hypertension. Methods and Results —Nineteen untreated patients with mild essential hypertension (47±2 years, range 30 to 65 years; 57% male) were randomly assigned in double-blind fashion to losartan or atenolol treatment for 1 year. Nine age/sex-matched normotensive subjects were also studied. Both treatments reduced blood pressure to a comparable degree (losartan, from 149±4.1/101±1.6 to 128±3.6/86±2.2 mm Hg, P <0.01; atenolol, from 150±4.0/99±1.2 to 130±3.2/84±1.4 mm Hg, P <0.01). Resistance arteries (luminal diameter 150 to 350 μm) dissected from gluteal subcutaneous biopsies were studied on a pressurized myograph. After 1 year of treatment, the ratio of the media width to lumen diameter of arteries from losartan-treated patients was significantly reduced (from 8.4±0.4% to 6.7±0.3%, P <0.01). Arteries from atenolol-treated patients exhibited no significant change (from 8.3±0.3% to 8.8±0.5% after treatment). Endothelium-dependent relaxation (acetylcholine-induced) was normalized by losartan (from 82.1±4.9% to 94.7±1.1%, P <0.01) but not by atenolol (from 80.4±2.7% to 81.7±4.6%). Endothelium-independent relaxation (by sodium nitroprusside) was unchanged after treatment. Conclusions —The AT 1 antagonist losartan corrected the altered structure and endothelial dysfunction of resistance arteries from patients with essential hypertension, whereas the β-blocker atenolol had no effect.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Echocardiographic assessment of left ventricular hypertrophy: Comparison to necropsy findings
Devereux, R. B., Alonso, D. R., Lutas, E. M., Gottlieb, G. J., Campo, E., Sachs, I., & Reichek, N. (1986) · The American Journal of Cardiology · doi:10.1016/0002-9149(86)90771-x · Cited by 6,229
Blood pressure, stroke, and coronary heart disease
Collins, R., Peto, R., MacMahon, S., Godwin, J., Qizilbash, N., Collins, R., MacMahon, S., Hebert, P., Eberlein, K. A., Taylor, J. O., et al. (1990) · The Lancet · doi:10.1016/0140-6736(90)90944-z · Cited by 4,491
The Pathogenesis of Coronary Artery Disease and the Acute Coronary Syndromes
Epstein, F. H., Fuster, V., Badimon, L., Badimon, J. J., & Chesebro, J. H. (1992) · New England Journal of Medicine · doi:10.1056/nejm199201303260506 · Cited by 3,725
Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells.
Griendling, K. K., Minieri, C. A., Ollerenshaw, J. D., & Alexander, R. W. (1994) · Circulation Research · doi:10.1161/01.res.74.6.1141 · Cited by 2,735
The Pathogenesis of Coronary Artery Disease and the Acute Coronary Syndromes
Epstein, F. H., Fuster, V., Badimon, L., Badimon, J. J., & Chesebro, J. H. (1992) · New England Journal of Medicine · doi:10.1056/nejm199201233260406 · Cited by 2,717
Abnormal Endothelium-Dependent Vascular Relaxation in Patients with Essential Hypertension
Panza, J. A., Quyyumi, A. A., Brush, J. E., & Epstein, S. E. (1990) · New England Journal of Medicine · doi:10.1056/nejm199007053230105 · Cited by 2,367
Close Relation of Endothelial Function in the Human Coronary and Peripheral Circulations
Anderson, T. J., Uehata, A., Gerhard, M. D., Meredith, I. T., Knab, S., Delagrange, D., Lieberman, E. H., Ganz, P., Creager, M. A., Yeung, A. C., et al. (1995) · Journal of the American College of Cardiology · doi:10.1016/0735-1097(95)00327-4 · Cited by 2,033
Sokolow, M., & Lyon, T. P. (1949) · American Heart Journal · doi:10.1016/0002-8703(49)90562-1 · Cited by 1,980
The pathogenesis of coronary artery disease and the acute coronary syndromes (First of two parts)
Fuster, V. (1992) · New England Journal of Medicine · Cited by 1,954
Hypertension : pathophysiology, diagnosis, and management
Laragh, J. H., & Brenner, B. M. (1995) · Raven Press eBooks · Cited by 1,932
Cited by
Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system
Mehta, P. K., & Griendling, K. K. (2007) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00287.2006 · Cited by 1,924
Role of the T cell in the genesis of angiotensin II–induced hypertension and vascular dysfunction
Guzik, T. J., Hoch, N. E., Brown, K. A., McCann, L. A., Rahman, A., Dikalov, S., Goronzy, J., Weyand, C., & Harrison, D. G. (2007) · The Journal of Experimental Medicine · doi:10.1084/jem.20070657 · Cited by 1,736
The CAFE Investigators, CAFE Steering Committee and Writing Committee, Williams, B., Lacy, P. S., Thom, S. M., Cruickshank, K., Stanton, A., Collier, D., Hughes, A. D., Thurston, H., et al. (2006) · Circulation · doi:10.1161/circulationaha.105.595496 · Cited by 1,645
Oxidative Stress and Vascular Disease
Madamanchi, N. R., Vendrov, A., & Runge, M. S. (2005) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.0000150649.39934.13 · Cited by 1,618
Biomarkers of Cardiovascular Disease: Molecular Basis and Practical Considerations
Vasan, R. S. (2006) · Circulation · doi:10.1161/circulationaha.104.482570 · Cited by 1,212
Metadata
- Authors
- Schiffrin, E. L., Park, J. B., Intengan, H. D., & Touyz, R. M.
- Venue
- Circulation
- Published
- 2000-04-11
- Volume
- 101
- Issue
- 14
- Pages
- 1653-1659
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2082291507
- Cited by
- 616
- References
- 56
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Correction of Arterial Structure and Endothelial Dysfunction in Human Essential Hypertension by the Angiotensin Receptor Antagonist Losartan. https://app.cochat.ai/papers/10.1161/01.cir.101.14.1653
- The paper
- Schiffrin, E. L., Park, J. B., Intengan, H. D., & Touyz, R. M. (2000). Correction of Arterial Structure and Endothelial Dysfunction in Human Essential Hypertension by the Angiotensin Receptor Antagonist Losartan. Circulation. https://doi.org/10.1161/01.cir.101.14.1653
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.