(Circulation. 2000;101:1653.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Correction of Arterial Structure and Endothelial Dysfunction in Human Essential Hypertension by the Angiotensin Receptor Antagonist Losartan
From the Medical Research Council Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, University of Montreal, Montreal, Quebec, Canada.
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 (AT1) receptor antagonist losartan, in contrast to the ß-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 AT1 antagonist losartan corrected the altered structure and endothelial dysfunction of resistance arteries from patients with essential hypertension, whereas the ß-blocker atenolol had no effect.
Key Words: arteries • blood pressure • endothelium • hypertrophy • receptors • remodeling
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Y. Higashi, S. Sasaki, K. Nakagawa, M. Kimura, S. Sasaki, K. Noma, H. Matsuura, K. Hara, C. Goto, T. Oshima, et al. Excess Norepinephrine Impairs Both Endothelium-Dependent and -Independent Vasodilation in Patients With Pheochromocytoma Hypertension, February 1, 2002; 39(2): 513 - 518. [Abstract] [Full Text] [PDF]
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G. Nickenig and D. G. Harrison The AT1-Type Angiotensin Receptor in Oxidative Stress and Atherogenesis: Part I: Oxidative Stress and Atherogenesis Circulation, January 22, 2002; 105(3): 393 - 396. [Full Text] [PDF]
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J. C. Spratt, D. J Webb, A. Shiels, and B. Williams Effects of candesartan on cardiac and arterial structure and function in hypertensive subjects Journal of Renin-Angiotensin-Aldosterone System, December 1, 2001; 2(4): 227 - 232. [Abstract] [PDF]
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M. Imamura, S. Biro, T. Kihara, S. Yoshifuku, K. Takasaki, Y. Otsuji, S. Minagoe, Y. Toyama, and C. Tei Repeated thermal therapy improves impaired vascular endothelial function in patients with coronary risk factors J. Am. Coll. Cardiol., October 1, 2001; 38(4): 1083 - 1088. [Abstract] [Full Text] [PDF]
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L. M. Ruilope and E. L. Schiffrin Blood Pressure Control and Benefits of Antihypertensive Therapy: Does It Make a Difference Which Agents We Use? Hypertension, September 1, 2001; 38(3): 537 - 542. [Abstract] [Full Text] [PDF]
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R. M. Touyz, G. He, X.-H. Wu, J. B. Park, M. E. Mabrouk, and E. L. Schiffrin Src Is an Important Mediator of Extracellular Signal-Regulated Kinase 1/2-Dependent Growth Signaling by Angiotensin II in Smooth Muscle Cells From Resistance Arteries of Hypertensive Patients Hypertension, July 1, 2001; 38(1): 56 - 64. [Abstract] [Full Text] [PDF]
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J. B. Park and E. L. Schiffrin ETA Receptor Antagonist Prevents Blood Pressure Elevation and Vascular Remodeling in Aldosterone-Infused Rats Hypertension, June 1, 2001; 37(6): 1444 - 1449. [Abstract] [Full Text] [PDF]
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S. Wassmann, U. Laufs, A. T. Baumer, K. Muller, K. Ahlbory, W. Linz, G. Itter, R. Rosen, M. Bohm, and G. Nickenig HMG-CoA Reductase Inhibitors Improve Endothelial Dysfunction in Normocholesterolemic Hypertension via Reduced Production of Reactive Oxygen Species Hypertension, June 1, 2001; 37(6): 1450 - 1457. [Abstract] [Full Text] [PDF]
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J. C. Chambers, L. Fusi, I. S. Malik, D. O. Haskard, M. De Swiet, and J. S. Kooner Association of Maternal Endothelial Dysfunction With Preeclampsia JAMA, March 28, 2001; 285(12): 1607 - 1612. [Abstract] [Full Text] [PDF]
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M.-S. Zhou, A. Adam, and L. Raij Review: Interaction among angiotensin II, nitric oxide and oxidative stress Journal of Renin-Angiotensin-Aldosterone System, March 1, 2001; 2(1_suppl): S59 - S63. [PDF]
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R. M. Touyz, G. He, M. El Mabrouk, and E. L. Schiffrin p38 MAP Kinase Regulates Vascular Smooth Muscle Cell Collagen Synthesis by Angiotensin II in SHR But Not in WKY Hypertension, February 1, 2001; 37(2): 574 - 580. [Abstract] [Full Text] [PDF]
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 J. A.A. Borland, A. H. Chester, S. J. Rooker, J. Wharton, N. Davie, M. Amrani, and M. H. Yacoub Expression and function of angiotensin converting enzyme, chymase, and angiotensin II in the human radial artery and internal thoracic artery Ann. Thorac. Surg., December 1, 2000; 70(6): 2054 - 2063. [Abstract] [Full Text] [PDF]
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 R. M. Touyz and E. L. Schiffrin Signal Transduction Mechanisms Mediating the Physiological and Pathophysiological Actions of Angiotensin II in Vascular Smooth Muscle Cells Pharmacol. Rev., December 1, 2000; 52(4): 639 - 672. [Abstract] [Full Text] [PDF]
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B. Dahlof Valsartan and the renin-angiotensin-aldosterone system: blood pressure control and beyond Journal of Renin-Angiotensin-Aldosterone System, June 1, 2000; 1(2_suppl): S14 - S16. [Abstract] [PDF]
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N. K. Hollenberg Hypertension, Small Arteries, and Pathways for Angiotensin II Generation : "The Proper Study of Mankind is Man" Circulation, April 11, 2000; 101(14): 1641 - 1642. [Full Text] [PDF]
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