Does soluble epoxide hydrolase inhibition prevent coronary endothelial dysfunction in mice with renovascular hypertension?
These results demonstrate that a reduced EET-mediated relaxations related to an increased degradation by sEH contributes to coronary endothelial dysfunction in 2K1C hypertensive mice. Inhibiting sEH prevents endothelial dysfunction by restoring EET-mediated relaxations and thus, could represent a promising pharmacological intervention to limit cardiovascular morbidity and mortality in arterial hypertension.
Even though the pharmacists' recommendations were followed in many cases in an ED, there is still room for improvement, especially for the surgical patients.