Hypertension — a major risk factor for stroke, myocardial infarction and heart failure — affects about 1.4 billion people worldwide and is poorly controlled in a third of patients despite treatment with multiple drugs.
Sergey Dikalov, PhD, and colleagues explored the role of mitochondrial oxidative stress and cytotoxic lipid oxidation products called isolevuglandins in hypertension. They showed that mitochondrial isolevuglandins accumulate in arterioles of patients with essential hypertension and in mice with angiotensin II-induced hypertension.
A novel molecule they developed (mito2HOBA) that “scavenges” mitochondrial isolevuglandins reduced oxidative stress and improved mitochondrial antioxidant activity in isolated human arterioles and cultured cells. It also attenuated hypertension in a mouse model.
The findings, reported in the journal Hypertension, support the role of mitochondrial isolevuglandins in endothelial dysfunction and hypertension. Using a “scavenger” such as mito2HOBA to prevent the damaging actions of isolevuglandins may have therapeutic potential for treating vascular dysfunction and hypertension, the authors concluded.
This research was supported by the National Institutes of Health (grants HL124116, HL144943, HL129941, GM129662, GM112871), American Heart Association and Navicent Health Foundation.
