The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Acute and Chronic Angiotensin-1 Receptor Antagonism Reverses Endothelial Dysfunction in Atherosclerosis
Open accessAbstract
Background —The renin-angiotensin system may contribute to atherogenesis through the promotion of endothelial dysfunction. The present study was performed to determine whether angiotensin-1 (AT 1 ) receptor inhibition improves endothelial dysfunction. Methods and Results —In the femoral circulation of 19 patients with atherosclerosis and of 9 control subjects, we studied microvascular responses to reactive hyperemia, angiotensin II, acetylcholine, and sodium nitroprusside before and after the administration of intra-arterial losartan (10 mg). Femoral artery flow velocity was measured with a Doppler flow wire, and the femoral vascular resistance index (FVRI) was calculated as mean arterial pressure divided by flow velocity. Losartan induced a minor (5.9±2%, P =0.02) reduction in FVRI and inhibited angiotensin II–mediated vasoconstriction in both patient groups ( P <0.01). After the administration of losartan, acetylcholine-mediated vasodilation was augmented in patients (44±5% to 58±4% reduction in FVRI with infusion at a rate of 150 μg/min, P <0.001) but not control subjects. Vasodilation during reactive hyperemia was also greater after AT 1 receptor inhibition ( P =0.03) in patients, but the response to sodium nitroprusside remained unchanged. In a separate group of 31 patients with atherosclerosis, we investigated the effect of 8 weeks of oral losartan therapy on brachial artery flow-mediated vasodilation with the use of high-resolution ultrasound. Oral losartan therapy improved flow-mediated brachial artery dilation (1.4±0.9% to 3.2±0.8%, P =0.03) but had no effect on the nitroglycerin response. Serum nitrogen oxide levels increased from 21.6±1.7 to 26.7±2.4 μmol/L ( P =0.008). Conclusions —The results of the present study indicate that inhibition of the AT 1 receptor in patients with atherosclerosis reverses endothelial dysfunction by improving NO availability and therefore may have long-term therapeutic benefits.
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Cites
Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis
Celermajer, D. S., Sorensen, K. E., Gooch, V. M., Spiegelhalter, D. J., Miller, O. I., Sullivan, I. D., Lloyd, J. K., & Deanfield, J. E. (1992) · The Lancet · doi:10.1016/0140-6736(92)93147-f · Cited by 4,742
Cited by
The clinical implications of endothelial dysfunction
Widlansky, M. E., Gokce, N., Keaney, J. F., & Vita, J. A. (2003) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(03)00994-x · Cited by 1,749
Endothelial Dysfunction and Hypertension
Konukoglu, D., & Uzun, H. (2016) · Advances in Experimental Medicine and Biology · doi:10.1007/5584_2016_90 · Cited by 594
Vascular inflammation and the renin-angiotensin system
Brasier, A. R., Recinos, A., & Eledrisi, M. S. (2002) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.0000021412.56621.a2 · Cited by 586
Renin-angiotensin-aldosterone system and oxidative stress in cardiovascular insulin resistance
Cooper, S. A., Whaley-Connell, A., Habibi, J., Wei, Y., Lastra, G., Manrique, C., Stas, S., & Sowers, J. R. (2007) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00522.2007 · Cited by 317
Ceriello, A., Assaloni, R., Da Ros, R., Maier, A., Piconi, L., Quagliaro, L., Esposito, K., & Giugliano, D. (2005) · Circulation · doi:10.1161/01.cir.0000165070.46111.9f · Cited by 298
Metadata
- Authors
- Prasad, A., Tupas-Habib, T., Schenke, W. H., Mincemoyer, R., Panza, J. A., Waclawin, M. A., Ellahham, S., & Quyyumi, A. A.
- Venue
- Circulation
- Published
- 2000-05-23
- Volume
- 101
- Issue
- 20
- Pages
- 2349-2354
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2092976211
- Cited by
- 196
- References
- 1
- FWCI
- 13.87
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Acute and Chronic Angiotensin-1 Receptor Antagonism Reverses Endothelial Dysfunction in Atherosclerosis. https://app.cochat.ai/papers/10.1161/01.cir.101.20.2349
- The paper
- Prasad, A., Tupas-Habib, T., Schenke, W. H., Mincemoyer, R., Panza, J. A., Waclawin, M. A., Ellahham, S., & Quyyumi, A. A. (2000). Acute and Chronic Angiotensin-1 Receptor Antagonism Reverses Endothelial Dysfunction in Atherosclerosis. Circulation. https://doi.org/10.1161/01.cir.101.20.2349
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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).
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