| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 1995;26:509-513.)
© 1995 American Heart Association, Inc.
Articles |
Sick Vessel Syndrome
Recovery of Atherosclerotic and Hypertensive Vessels
From the Departments of Internal Medicine, Pharmacology, and Pathology, Cardiovascular Center and Center on Aging, College of Medicine and Veterans Administration Medical Center, Iowa City.
Correspondence to Donald D. Heistad, MD, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, IA 52242.
Abstract This review describes vascular changes in atherosclerotic and hypertensive vessels as well as effects of treatment. Changes in vascular structure in both atherosclerosis and hypertension are characterized by thickening of the vessel wall and vascular "remodeling." Remodeling tends to preserve the size of the lumen in atherosclerotic vessels and results in a smaller lumen in hypertensive vessels. Changes in vascular function are characterized by preservation of smooth muscle relaxation, with the exception of activity of ATP-sensitive potassium channels, and dysfunction of endothelium. Regression of atherosclerosis, by treatment of hyperlipidemia, results in quite rapid removal of lipid from the vessel wall but with inconsistent improvement in maximal vasodilator capacity. In contrast, endothelial function improves during regression of atherosclerosis, and hyperresponsiveness to serotonin subsides rapidly. Effective treatment of hypertension produces regression of vascular hypertrophy, and some approaches (especially angiotensin-converting enzyme inhibitors) are effective in correcting vascular remodeling. Endothelium-dependent relaxation generally improves during antihypertensive treatment. Reduction in pulse pressure may be more important than reduction in mean arterial pressure in reversing the structural and functional abnormalities of hypertensive vessels.
Key Words: vascular remodeling • hypertension • endothelium • atherosclerosis • vascular hypertrophy
This article has been cited by other articles:
 |
|
 |
|
  J. R. Jennings, M. F. Muldoon, C. Ryan, J. C. Price, P. Greer, K. Sutton-Tyrrell, F. M. van der Veen, and C. C. Meltzer Reduced cerebral blood flow response and compensation among patients with untreated hypertension Neurology, April 26, 2005; 64(8): 1358 - 1365. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Cediel, D. Sanz-Rosa, M. P. Oubina, N. de las Heras, F. R. G. Pacheco, O. Vegazo, J. Jimenez, V. Cachofeiro, and V. Lahera Effect of AT1 receptor blockade on hepatic redox status in SHR: possible relevance for endothelial function? Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2003; 285(3): R674 - R681. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Laurent, S. Katsahian, C. Fassot, A.-I. Tropeano, I. Gautier, B. Laloux, and P. Boutouyrie Aortic Stiffness Is an Independent Predictor of Fatal Stroke in Essential Hypertension Stroke, May 1, 2003; 34(5): 1203 - 1206. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. S. Stokes, E. S. Barin, and K. L. Gilfillan Effects of Isosorbide Mononitrate and AII Inhibition on Pulse Wave Reflection in Hypertension Hypertension, February 1, 2003; 41(2): 297 - 301. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Domanski, B. R. Davis, M. A. Pfeffer, M. Kastantin, and G. F. Mitchell Isolated Systolic Hypertension : Prognostic Information Provided by Pulse Pressure Hypertension, September 1, 1999; 34(3): 375 - 380. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. deBlois, B.-S. Tea, T.-V. Dam, J. Tremblay, and P. Hamet Smooth Muscle Apoptosis During Vascular Regression in Spontaneously Hypertensive Rats Hypertension, January 1, 1997; 29(1): 340 - 344. [Abstract] [Full Text] [PDF]
|
|