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Hemodynamic determinants of vascular changes in hypertension and atherosclerosis
D D Heistad1, J A Lopez, G L Baumbach
1Department of Internal Medicine, Veterans Administration Medical Center, Iowa City, Iowa.
Insights
Lowering blood pressure may slow atherosclerosis progression. Both atherosclerosis and hypertension cause vascular remodeling, but with different effects on blood vessel lumen size. Functional changes impair vasodilation, and leukocytes and platelets may mediate spasms.
Area of Science:
- Cardiovascular Science
- Vascular Biology
- Pathophysiology
Background:
- Atherosclerosis and hypertension are major cardiovascular diseases characterized by vascular changes.
- Understanding the structural and functional alterations in blood vessels is crucial for managing these conditions.
Purpose of the Study:
- To review new concepts regarding structural and functional changes in atherosclerotic and hypertensive blood vessels.
- To explore the implications of blood pressure modulation on vascular changes.
- To differentiate the effects of vascular remodeling in atherosclerosis versus hypertension.
Main Methods:
- Review of current scientific literature on vascular remodeling and function.
- Analysis of structural and functional adaptations in blood vessels under different pressure conditions.
- Examination of cellular mediators involved in vascular spasm.
Main Results:
- Atherosclerosis progression is slower during hypotension compared to normotension, suggesting implications for optimal blood pressure.
- Vascular remodeling occurs in both conditions: preserving lumen in atherosclerosis but reducing it in hypertension.
- Impaired active vasodilator responses, partly endothelium-dependent, are observed in both atherosclerotic and hypertensive vessels.
- Leukocytes and platelets are proposed as potential mediators of spasm in atherosclerotic arteries.
Conclusions:
- Blood pressure management may influence atherosclerosis progression.
- Vascular remodeling has distinct consequences in atherosclerosis and hypertension.
- Endothelium-dependent mechanisms contribute to impaired vasodilation in these diseases.
- Cellular mediators like leukocytes and platelets warrant further investigation for their role in vascular spasm.
Abstract:
Several new concepts are reviewed concerning structural and functional changes in atherosclerotic and hypertensive blood vessels. First, in regard to modulation of vascular changes, atherosclerosis appears to progress more slowly during hypotension than during normotension. This finding may have implications for the optimal level of blood pressure. Second, structural "remodeling" of the vessel wall occurs in both atherosclerosis and hypertension. Remodeling helps to preserve the arterial lumen despite intimal proliferation in atherosclerosis. In contrast, remodeling (which differs from vascular hypertrophy) reduces the vascular lumen in chronic hypertension. Third, functional changes impair active vasodilator responses in both atherosclerotic and hypertensive vessels, in part by endothelium-dependent mechanisms. Finally, we propose that leukocytes as well as platelets may be important cellular mediators of spasm in atherosclerotic arteries.