title: Insulin resistance and associated dysfunction of resistance vessels and arterial hypertension.
abstract: Insulin resistance (IR) has profound, negative effects on the function of arteries and arterioles throughout the body and leads to arterial hypertension and vascular occlusive diseases such as heart attacks and strokes. IR affects arteries and arterioles at both the endothelium and smooth muscle levels. One major, underlying mechanism of vascular dysfunction appears to involve the augmented generation, availability and subsequent actions of reactive oxygen species (ROS). Thus, application of superoxide dismutase (SOD), a specific scavenger of superoxide anion, is able to immediately restore normal dilator responsiveness in IR arteries. In some but not all circulations, however, other factors such as increased production of and actions by constrictor agents such as endothelin also appear to restrict normal dilator responses. The basis of ROS-mediated vascular dysfunction in IR is not completely understood, but inflammatory processes throughout the arterial wall appear to be involved. Treatments involving behavioral approaches, such as changes in diet, weight loss, and regular exercise, and pharmacological approaches, involving the use of insulin-sensitizing agents or statins, appear to offer benefits against the detrimental vascular effects of IR. Nonetheless, the most effective approach appears to involve prevention of IR via adoption of a healthy lifestyle by young people.
authors.affiliation: Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, NC 27157, USA. dbusija@wfubmc.edu
authors.forename: D W
authors.initials: DW
authors.lastname: Busija
authors.forename: A W
authors.initials: AW
authors.lastname: Miller
authors.forename: P
authors.initials: P
authors.lastname: Katakam
authors.forename: B
authors.initials: B
authors.lastname: Erdös
mesh_terms: D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000517:prevention & control; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D015221:Potassium Channels / Q000502:physiology; D051381:Rats; D011924:Rats, Zucker; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000494:pharmacology; D014655:Vascular Resistance / Q000502:physiology; D014664:Vasodilation / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D015221:Potassium Channels; D017382:Reactive Oxygen Species; D014665:Vasodilator Agents; D013482:Superoxide Dismutase