Does antihypertensive treatment reverse endothelial dysfunction in patients with human hypertension?
Endothelial dysfunction, driven by reduced nitric oxide availability, is a key mechanism of vascular damage in hypertension, and different antihypertensive classes vary in their ability to reverse it.
Endothelium-derived nitric oxide is not only a potent vasodilator but also inhibits platelet aggregation, smooth muscle cell proliferation, monocyte adhesion and adhesion molecule expression. In several pathological conditions, such as human hypertension, nitric oxide availability is reduced. This alteration has been documented in the peripheral and coronary micro- and macrocirculation and in the renal circulation. The main mechanism leading to endothelial dysfunction is production of cyclooxygenase-dependent factors, including prostanoids and oxygen free radicals, which cause nitric oxide breakdown. Dysfunctional endothelium can be one of the main mechanisms causing vascular damage, in particular, atherosclerosis; hence, an important aim for antihypertensive treatment could reside not only in normalizing blood pressure values but also in reversing endothelial dysfunction. Available evidence indicates that different classes of antihypertensive compounds have different effects on endothelial dysfunction.
Taddei et al. (Sun,) studied this question.