title: Effects of treatment strategy on endothelial function.
abstract: A large body of evidence indicates that endothelial dysfunction is a characteristic of patients with arterial hypertension. As functional abnormalities lead to impaired endothelium-dependent vasodilation, this early step of atherogenesis is potentially reversible. In addition to reducing blood pressure, the major families of anti-hypertensive drugs have a number of pleiotropic effects that could improve endothelial function. In particular, the renin-angiotensin system plays an important role in the pathogenesis of both arterial hypertension and endothelial dysfunction, and so drugs capable of limiting the dangerous effects of this hormonal axis, such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers and renin inhibitors, could help prevent/delay/reverse the atherosclerotic process. New third-generation β-blockers and 5-phosphodiesterase inhibitors may affect endothelial function. Furthermore, the HMGCoA-reductase inhibitors currently used to reduce cholesterol levels have major pleiotropic anti-inflammatory and anti-hypertensive effects. The preservation or recovery of endothelial function in hypertensive patients is crucial to inhibit the development of atherosclerosis and the onset of cardiovascular events. This review focuses on the ancillary effects of hypertensive drugs and HMGCoA-reductase inhibitors that go beyond lowering blood pressure and cholesterol levels.
authors.affiliation: IRCCS Galeazzi Orthopedic Institute, Department of Health Technologies, Università di Milano, Milan, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Tomasoni
authors.forename: S
authors.initials: S
authors.lastname: Sitia
authors.forename: C
authors.initials: C
authors.lastname: Borghi
authors.forename: A F G
authors.initials: AF
authors.lastname: Cicero
authors.forename: C
authors.initials: C
authors.lastname: Ceconi
authors.forename: F
authors.initials: F
authors.lastname: Cecaro
authors.forename: A
authors.initials: A
authors.lastname: Morganti
authors.forename: V
authors.initials: V
authors.lastname: De Gennaro Colonna
authors.forename: M
authors.initials: M
authors.lastname: Guazzi
authors.forename: L
authors.initials: L
authors.lastname: Morricone
authors.forename: A E
authors.initials: AE
authors.lastname: Malavazos
authors.forename: P
authors.initials: P
authors.lastname: Marino
authors.forename: C
authors.initials: C
authors.lastname: Cavallino
authors.forename: Y
authors.initials: Y
authors.lastname: Shoenfeld
authors.forename: M
authors.initials: M
authors.lastname: Turiel
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use; D050197:Atherosclerosis / Q000188:drug therapy* / Q000276:immunology; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D045462:Endothelium-Dependent Relaxing Factors / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D006973:Hypertension / Q000188:drug therapy* / Q000276:immunology; D007249:Inflammation; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000276:immunology
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000893:Anti-Inflammatory Agents; D000959:Antihypertensive Agents; D045462:Endothelium-Dependent Relaxing Factors; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors