title: The effect of antihypertensive drugs on vascular compliance.
abstract: Measurement of vascular compliance has assumed increasing importance as a marker of early disease of the vascular wall, a predictor of future vascular disease, and a way to monitor the effects of vasoactive agents on arterial wall stiffness. Vascular compliance can be estimated by several methods: measurement of the pulse pressure, or pulse pressure-stroke volume ratio; analysis of the systolic pulse wave augmentation index and the diastolic pulse wave contour; ultrasonic echo-tracking; and MRI. Because few comparative studies have been done, the physiologic significance of the measures of compliance obtained by each method is uncertain. Antihypertensive drugs may improve vascular compliance by reducing blood pressure, relaxing vascular smooth muscle, or promoting long-term effects on vascular smooth muscle and cardiomyocyte growth and remodeling. Angiotensin converting enzyme (ACE) inhibitors have been reported to improve vascular compliance in nearly all studies, suggesting a beneficial class effect independent of blood pressure reduction. Favorable changes in the vascular wall-lumen ratio of small vessels from subcutaneous gluteal biopsy specimens after treatment with ACE inhibitors and the persistence of improved vascular compliance after withdrawal of therapy indicate that these agents may produce long-term vascular remodeling. Although few studies have been done, angiotensin II receptor antagonists improve vascular compliance, possibly by blocking angiotensin II-mediated cell proliferation and increasing apoptosis via unopposed AT1 receptor stimulation. In contrast, calcium antagonists and beta-blockers have variable effects on vascular compliance, although beta-blockers with intrinsic sympathomimetic activity improve vascular compliance. Diuretics have little effect on vascular compliance beyond their blood pressure-lowering actions, except for spironolactone, which by improving vascular compliance may have contributed to the reduction in heart failure mortality seen in the Randomized Aldactone Evaluation Study.
authors.affiliation: Division of Endocrinology, Diabetes, and Hypertension, SUNY Downstate Medical Center, Box 1205, 450 Clarkson Avenue, Brooklyn, NY 11203-2098, USA. nwiner@netmail.hscbklyn.edu
authors.forename: N
authors.initials: N
authors.lastname: Winer
authors.forename: M A
authors.initials: MA
authors.lastname: Weber
authors.forename: J R
authors.initials: JR
authors.lastname: Sowers
mesh_terms: D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000503:physiopathology*; D003187:Compliance / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology*; D006801:Humans
chemical_list: D000959:Antihypertensive Agents